3.1 Health and well-being

A biological explanation accounts for a psychological or health outcome through mechanisms such as genes, brain systems, hormones or neurotransmitters. It should specify how the mechanism could produce the observed change.

Biological evidence can be persuasive when converging methods agree, but reductionism may ignore cognition, learning and context. A biological association is not automatically a necessary or sufficient cause.

If a treatment changes serotonin signalling and symptoms change, the result supports a possible pathway but does not prove one neurotransmitter caused the disorder. Dose, placebo, adherence and side effects also matter.

‘Biological’ does not mean deterministic and ‘chemical imbalance’ is not a complete explanation. State the evidence, mechanism and alternative levels of analysis.

A cognitive model represents how information is noticed, interpreted, stored or used to guide behaviour. It is a testable simplification, not a literal map of every mental process.

Models generate predictions about attention, memory, appraisal and decision-making. Their usefulness depends on what they explain, what they omit and whether different tasks or populations produce the same pattern.

A person who interprets a neutral bodily sensation as danger may attend to more symptoms and remember alarming examples, increasing avoidance. Changing the appraisal can alter the cycle without claiming that the symptom was imaginary.

A model is not a diagnosis and a cognitive explanation does not deny biology. Identify the representation and process that link the situation to the health outcome.

Cultural differences in health may reflect beliefs, language, norms, access and measurement as well as biology. The same symptom or diagnostic label can carry different meanings in different settings.

An imposed diagnostic category may show culture bias if it treats one group's expression as the universal norm. Compare prevalence only after checking sampling, translation, help-seeking and whether the construct is equivalent.

If anxiety is reported less often in one group but somatic symptoms more often, the difference may reflect expression or access rather than less distress. A culturally adapted interview can reveal what a score alone misses.

A group average is not a cultural essence. Avoid stereotyping; identify the mechanism and the evidence needed to separate biology, context, reporting and diagnostic bias.

Environmental explanations focus on conditions around a person—stressors, resources, pollution, social support, discrimination, routines and learned opportunities—that can alter health behaviour or physiology.

Environment is not a single variable. A causal account must identify the exposure, pathway, timing and comparison, while considering selection and reverse causation. The same setting can protect one person and burden another.

A noisy housing area may reduce sleep through repeated disturbance, which can affect concentration and stress. Measuring noise, sleep and baseline health is stronger than attributing every difference to ‘the environment’.

Environmental does not mean non-biological: exposures can change biological processes. Identify the exposure, its timing and dose, the pathway to symptoms, and competing explanations before drawing a causal conclusion.

Prevalence is the proportion of a population with a condition at a specified time or period. Incidence counts new cases over time. Both need a numerator, denominator, case definition and date before comparisons are meaningful.

Prevalence rises when incidence increases or when people live longer with the condition, and falls when recovery or death removes cases. Survey method, diagnosis and access can change the measured rate without changing underlying health.

If 80 of 2,000 adults meet a defined criterion on a survey date, point prevalence is 4%. Comparing that with another country requires aligned age groups, instruments, sampling and dates.

Prevalence is not automatically risk or cause. A high value can reflect better detection or longer survival, so interpret the denominator and time window.

Social learning theory explains behaviour through observation, imitation and the social consequences attached to a model. Vicarious reinforcement changes expectations even when the observer is not directly rewarded.

Attention, retention, reproduction and motivation mediate whether an observed behaviour is learned and performed. The model's status, similarity and context influence what is noticed and whether imitation is feasible.

A teenager who sees a respected peer praised for using a bike helmet may remember the behaviour and adopt it later. The example supports a pathway, not a guarantee: access, skills and social norms still constrain action.

Seeing a behaviour is not the same as performing it, and correlation between media exposure and health behaviour does not prove imitation caused it. Name the mediating process.

Stress is a response to demands judged to exceed available resources. The HPA axis and cortisol help mobilise energy during challenge, but repeated or prolonged activation can disrupt sleep, immunity and metabolic regulation.

Acute stress can be adaptive; chronic stress depends on duration, controllability, appraisal and recovery. Cortisol measurements have timing and sampling limits, so a single value is not a complete stress diagnosis.

A demanding shift followed by adequate sleep may produce a temporary cortisol rise that returns toward baseline. Unpredictable demands with little recovery can maintain arousal and alter appetite or concentration over time.

Cortisol is not simply the ‘stress hormone’ that explains every illness. Separate exposure, appraisal, physiological response and health outcome, and consider individual and social moderators.

A biological treatment changes a bodily process—through medication, surgery or another physiological intervention—to reduce symptoms or risk. Its rationale should specify the target, expected pathway and time course.

Evidence needs an appropriate comparison, clinically meaningful outcome and attention to adherence, placebo effects, side effects and relapse. A statistical difference does not guarantee that benefits outweigh harms for every patient.

An antidepressant may alter neurotransmission and reduce symptoms for some patients, while delayed onset or adverse effects affect adherence. Combining medication with psychological or social support may address mechanisms the drug cannot.

A biological treatment is not automatically more objective or curative. A plausible mechanism is only one part of the evidence and does not erase informed choice.

Prevention aims to reduce risk before a problem develops; treatment responds after a condition is present. Public-health, psychological and technological interventions can target behaviour, exposure, access or recovery.

A prevention plan should name the target population, mechanism and outcome, then monitor reach and unintended effects. Digital tools can improve access or self-monitoring, but privacy, engagement and unequal access can change their impact.

A screening app may prompt early help-seeking, while a therapy platform may support treatment. Neither works simply because it is digital: evidence must show who uses it, what changes and whether harms or exclusion occur.

Prevention is not the same as treatment and an intervention's availability is not its effectiveness. Separate mechanism, uptake, outcome and equity.

A psychological treatment uses structured psychological processes—such as cognitive reappraisal, behavioural practice, exposure, problem-solving or therapeutic relationship—to reduce symptoms or improve functioning.

A credible evaluation specifies the target mechanism, comparison, outcome and follow-up. Treatment response can vary with diagnosis, therapist skill, expectancy, adherence and context, so one trial does not establish universal superiority.

CBT for anxiety may identify catastrophic predictions, test them with graded behavioural experiments and track avoidance. Improvement is evidence about the treatment package, not proof that one thought caused every symptom.

Talking therapy is not a single intervention and improvement is not automatically a placebo effect. Match the treatment to a specified disorder, explain its active psychological process, and evaluate benefits, harms, access, relapse and patient preference.

An interview is a researcher–participant conversation used to collect self-report data. Structured interviews standardise questions; semi-structured interviews use a guide but allow probing; unstructured interviews follow the participant's account more freely.

Question wording, rapport, order, recording and reflexivity affect what is said and how it is interpreted. Pilot the schedule, protect confidentiality and obtain informed consent, especially when topics are sensitive.

A semi-structured interview about sleep can ask the same core questions while probing an unexpected routine. Two researchers can compare coding, but agreement does not remove social-desirability or interviewer effects.

Rich quotations do not automatically make findings valid. State the sampling, interview format, analysis and ethical safeguards before judging credibility or transferability.

A practical workflow is: define a focused health question; choose structured, semi-structured or focus-group format; recruit an appropriate sample; prepare neutral, open questions and prompts; pilot and revise the schedule; obtain informed consent and agree recording/confidentiality; conduct without leading; debrief and provide support information for sensitive topics; transcribe or summarize consistently; then code and report themes with reflexive notes and anonymized evidence.