Human Growth, Development and Maturation: Definitions and Principles, Prenatal and Postnatal Phases, the Distance, Velocity, Acceleration and Scammon Curves, Catch-Up and Catch-Down Growth, Ageing and Senescence, Somatic, Skeletal and Dental Maturation, Genetic and Environmental Factors, Secular Trends, the Methods of Growth Study and Body Composition

Growth is increase in size — in the number and size of cells and in the mass of intercellular material — measured as height, weight, limb lengths and circumferences. Development is increase in complexity and function: differentiation of tissues, the acquisition of skills, the maturing of organ systems. Maturation is progress toward the adult state along a timetable that is partly independent of size: two children of the same height may be years apart in skeletal or sexual maturity. Human growth follows regular principles. It is continuous but not uniform, fast in infancy, slow in childhood, fast again at adolescence and then ceasing. It proceeds cephalocaudally (head first — the head is a quarter of body length at birth and an eighth in the adult) and proximodistally (trunk before limbs; in the adolescent spurt, however, feet and hands enlarge before the legs and arms, and the limbs before the trunk). Different tissues grow at different rates (Scammon), and growth has a strong genetic timetable — the "target-seeking" or canalised property that Waddington and Tanner described, which is what makes catch-up possible. The pattern is species-specific: compared with other primates, humans add a long childhood and an adolescent growth spurt, the stages Bogin sets out as infancy (to weaning at about three years), childhood (three to seven), juvenile (seven to puberty), adolescence (the spurt to adult size) and adulthood. Physical growth stops when the epiphyses of the long bones fuse, at about 16–18 years in girls and 18–20 in boys.

Prenatal growth has three phases: the ovum or germinal period (fertilisation to implantation, the first two weeks), the embryonic period (weeks three to eight, when all organ systems are laid down and the embryo is most vulnerable to teratogens) and the fetal period (week nine to birth, growth in size). Length velocity peaks at about the fourth month, weight velocity at about the eighth; the average newborn is about 50 cm and 3.2–3.4 kg, and low birth weight is under 2,500 g. Postnatal growth is fastest in the first year (about 25 cm in length, weight tripled), slows through childhood to 5–6 cm a year with a small mid-growth spurt at six to eight years, and then accelerates in the adolescent spurt — peak height velocity about 9 cm a year in boys at 14 and about 8 cm a year in girls at 12, girls starting about two years earlier and finishing earlier, which is why adult men are taller. Body parts grow on different schedules: the brain and head near adult size by seven; the lymphoid tissue overshooting in childhood; the reproductive organs dormant until puberty; the legs growing proportionately more than the trunk in childhood, the trunk catching up at adolescence. Subcutaneous fat, measured by skinfold calipers at the triceps and subscapular sites, rises in the first year, falls to a minimum at about five to seven (the "adiposity rebound" marks the turn), and then diverges: girls continue to add fat through adolescence, boys lose limb fat during their spurt and gain muscle. Physiological variables follow their own curves — heart rate falls from about 120 at birth to 70 in the adult while blood pressure rises; basal metabolic rate per kilogram falls; haemoglobin dips in infancy and rises again, higher in boys after puberty; muscle strength surges after peak height velocity in boys, about a year later than the height spurt.

A distance curve plots the size attained (height in cm) against age: a rising S-shaped line — steep in infancy, gently sloping in childhood, steep again at adolescence, flat in adulthood. A velocity curve plots the rate of growth (cm per year) against age: high at birth and falling through infancy, low and slowly declining through childhood, rising to the adolescent peak and falling to zero. An acceleration curve plots the change in velocity: it is positive when velocity is increasing (the start of the spurt) and negative when velocity is falling (after peak height velocity), crossing zero at the peak. Tanner's Growth at Adolescence (1962) made these three the standard. Velocity is more sensitive than distance to short-term influences such as illness or famine, and the individual's velocity curve is sharper than the population's "mean-constant" curve, which smears the spurt across the range of ages at which children reach it. Richard Scammon (1930) showed that the body's tissues follow four different curves when each is plotted as a percentage of its adult size: the general (or somatic) curve of height, weight, muscle, skeleton and viscera, sigmoid with the adolescent spurt; the neural curve of brain, skull, eyes and ears, which reaches about 90% of adult size by six to seven and is complete by ten; the lymphoid curve of thymus, tonsils, lymph nodes and gut lymphoid tissue, which overshoots to nearly 200% of the adult value at about eleven to twelve and then involutes; and the genital curve of the gonads and reproductive organs, which is nearly flat until puberty and then rises steeply. Catch-up growth (Prader, Tanner and von Harnack, 1963) is the acceleration above the normal velocity that follows the removal of a growth-restraining cause — an illness cured, a famine ended, a hormone replaced — restoring the child to its genetic trajectory or "channel"; it is complete if the restraint was brief and mild, incomplete if it fell in infancy or lasted long. Catch-down growth is the mirror: a large infant whose growth was pushed above its channel by maternal factors decelerates in the first years to settle on its genetic line. Both express the canalisation of growth.

Ageing is the passage of time in the organism; senescence is the progressive, irreversible decline in function and in the capacity to repair that follows maturity — loss of stature through vertebral compression and postural change, loss of bone mineral (osteoporosis, faster in post-menopausal women), loss of muscle (sarcopenia), redistribution of fat to the trunk, declining vital capacity, cardiac output, renal clearance and hearing, greying and hair loss, menopause at about 50. Theories of senescence are programmed (the Hayflick limit and telomere shortening; the endocrine clock) and stochastic (accumulated damage from free radicals, errors and cross-linking; the disposable-soma theory of Kirkwood). Maturation is assessed on three scales. Somatic maturity is judged by the proportion of adult height attained, by peak height velocity and by the secondary sexual characters graded in Tanner's five stages. Skeletal maturity, the most reliable, is read from radiographs of the left hand and wrist against a standard atlas — Greulich and Pyle (1959) — or by scoring each bone as in the Tanner–Whitehouse (TW2, TW3) method; it gives a "bone age" that can be compared with chronological age, and epiphyseal fusion marks the end of growth. Dental maturity is read from tooth eruption — the 20 deciduous teeth from about six months to two and a half years, the 32 permanent teeth from six years (first molar) to the third molars at 17–25 — and, more precisely, from the calcification stages of the teeth on radiographs (Demirjian, 1973); it is the least affected by malnutrition and the most useful in forensic age estimation. Growth is the outcome of genes and environment together. Genetic factors set the target and the tempo: heritability of adult height is about 0.8, parent–child correlations are about 0.5, twin studies show MZ pairs far more alike than DZ, and populations differ (the pygmies' low growth-hormone receptor response, the tall Nilotes). Environmental factors decide how much of the target is reached: nutrition (protein-energy malnutrition stunts; the Indian NFHS-5 of 2019–21 found about 36% of under-fives stunted), infection (diarrhoea and malaria divert energy), socio-economic status, family size, urban residence, altitude, climate and season (children grow faster in height in spring, in weight in autumn), psychosocial stress (deprivation dwarfism) and hormones (growth hormone, thyroxine, sex steroids, insulin). Secular trends are changes in growth from one generation to the next: over the last 150 years children in industrialised countries have grown taller at every age and matured earlier — adult height up by about 1 cm a decade, menarche down from about 16–17 to about 12.5–13 — attributed to nutrition, health and smaller families; the trend has plateaued in the richest countries and is now visible in urban India, and a negative secular trend appears where conditions worsen.

A cross-sectional study measures many children of different ages once, each child contributing one point: quick and cheap, it yields population standards (the distance curve and its centiles — the WHO 2006 standards, the Indian ICMR and IAP charts) but cannot show an individual's velocity or the timing of the spurt, which it blurs into the mean-constant curve. A longitudinal study follows the same children over years, measuring each repeatedly: it gives true velocity and acceleration curves, the age at take-off and peak, and the effects of events, but it is slow, costly, loses subjects and is vulnerable to a secular trend during its course (the Harpenden study of Tanner, the Fels study, the Guidance studies, and in India the New Delhi birth cohort begun in 1969). A mixed-longitudinal study is the compromise: several overlapping age cohorts are each followed for a few years — say children aged 0, 3, 6, 9 and 12 each followed for four years — so that the whole span from 0 to 16 is covered in four years with some longitudinal information in each segment. A linked-longitudinal study links successive short cohorts end to end so that each cohort's last year coincides with the next's first, allowing the segments to be joined into a single continuous growth curve while the study is kept short. Body composition divides the body into compartments. The two-compartment model of fat mass and fat-free (lean) mass is estimated from skinfolds (Durnin and Womersley's equations; the sum of four skinfolds), from body density by underwater weighing (Siri's equation: % fat = 495 ÷ density − 450), from bioelectrical impedance, from dual-energy X-ray absorptiometry (DXA), which also gives bone mineral mass and content and regional or segmental fat, and from deuterium dilution of total body water. Per cent body fat is about 15% in young men and 25% in young women; the body mass index (weight in kg ÷ height in m²) classes adults as underweight below 18.5, normal 18.5–24.9, overweight 25–29.9 and obese 30 and over (the Asia-Pacific cut-offs used in India are 23 and 25), and waist circumference and the waist–hip ratio measure central fat. Bone mass rises to its peak in the twenties and falls thereafter; "body age" or biological age, in this context, is the age a person's composition and function correspond to on the reference curves, as against chronological age.