Genes change the dose
Clinical trials report what happens *on average*. But you are not an average. Pharmacogenomics studies how inherited differences in our genes change drug response — the foundation of personalized medicine. Many of these differences sit in the cytochrome P450 enzymes that break drugs down. A pharmacogenetic polymorphism can make someone a *poor metaboliser* (the drug builds up, risking toxicity) or an *ultra-rapid metaboliser* (the drug clears so fast it barely works).
Special populations
Some groups are systematically different from the trial average and are grouped as special populations. They are often *under-represented* in trials, so prescribers must reason carefully rather than copy a standard dose.
- Children — paediatric pharmacology reminds us a child is not a small adult: organs, enzymes, and body water differ with age, so doses are usually scaled by weight or body size, not simply halved.
- Older adults — geriatric pharmacology deals with declining kidney and liver function, more body fat, and several drugs at once, all raising the risk of interactions and accumulation.
- Pregnancy — a drug may cross to the fetus and act as a teratogen, harming development. Prescribing weighs the mother's need against fetal risk, often choosing better-studied older drugs.
- Impaired kidneys — when the kidneys clear a drug slowly, renal impairment dosing lowers the dose or lengthens the interval to prevent dangerous build-up.
The last mile: adherence
All the science above is wasted if the medicine is never actually taken. Medication adherence is how closely a patient follows the prescribed plan — and roughly half of people with long-term conditions do not take their medicines as directed. The reasons are human: side effects, cost, complicated schedules, feeling well and forgetting, or simply not understanding why it matters.