OBJECTIVE:To review the empirical evidence of associations between television (TV) viewing, video/computer game use and (a) body fatness, and (b) physical activity. DESIGN: Meta-analysis. METHOD: Published English-language studies were located from computerized literature searches, bibliographies of primary studies and narrative reviews, and manual searches of personal archives. Included studies presented at least one empirical association between TV viewing, video/computer game use and body fatness or physical activity among samples of children and youth aged 3-18 y. MAIN OUTCOME MEASURE: The mean sample-weighted corrected effect size (Pearson r). RESULTS: Based on data from 52 independent samples, the mean sample-weighted effect size between TV viewing and body fatness was 0.066 (95% CI ¼ 0.056-0.078; total N ¼ 44 707). The sample-weighted fully corrected effect size was 0.084. Based on data from six independent samples, the mean sample-weighted effect size between video/computer game use and body fatness was 0.070 (95% CI ¼ À0.048 to 0.188; total N ¼ 1722). The sample-weighted fully corrected effect size was 0.128. Based on data from 39 independent samples, the mean sample-weighted effect size between TV viewing and physical activity was À0.096 (95% CI ¼ À0.080 to À0.112; total N ¼ 141 505). The sample-weighted fully corrected effect size was À0.129. Based on data from 10 independent samples, the mean sample-weighted effect size between video/computer game use and physical activity was À0.104 (95% CI ¼ À0.080 to À0.128; total N ¼ 119 942). The sample-weighted fully corrected effect size was À0.141. CONCLUSION: A statistically significant relationship exists between TV viewing and body fatness among children and youth although it is likely to be too small to be of substantial clinical relevance. The relationship between TV viewing and physical activity is small but negative. The strength of these relationships remains virtually unchanged even after correcting for common sources of bias known to impact study outcomes. While the total amount of time per day engaged in sedentary behavior is inevitably prohibitive of physical activity, media-based inactivity may be unfairly implicated in recent epidemiologic trends of overweight and obesity among children and youth. Relationships between sedentary behavior and health are unlikely to be explained using single markers of inactivity, such as TV viewing or video/computer game use.

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Our equations provided good fits in external samples and provide an alternative to commonly used models. Original prediction equations were simplified with no meaningful increase in estimation error.

Homo naledi is a previously-unknown species of extinct hominin discovered within the Dinaledi Chamber of the Rising Star cave system, Cradle of Humankind, South Africa. This species is characterized by body mass and stature similar to small-bodied human populations but a small endocranial volume similar to australopiths. Cranial morphology of H. naledi is unique, but most similar to early Homo species including Homo erectus, Homo habilis or Homo rudolfensis. While primitive, the dentition is generally small and simple in occlusal morphology. H. naledi has humanlike manipulatory adaptations of the hand and wrist. It also exhibits a humanlike foot and lower limb. These humanlike aspects are contrasted in the postcrania with a more primitive or australopith-like trunk, shoulder, pelvis and proximal femur. Representing at least 15 individuals with most skeletal elements repeated multiple times, this is the largest assemblage of a single species of hominins yet discovered in Africa.

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The secular trends in height, sitting height and leg length in Japanese children have been studied by fitting Preece-Baines Model I curves to the annual mean values from ages five to 17 of school data collected in 1957, 1967 and 1977. The method provides estimates of final adult value, and of age of maximum annual increment. Between 1957 and 1977 the maximal increments in height, sitting height and leg length all became earlier, by about a year in boys and a little less in girls. Japanese now mature about a year earlier than North Europeans. Adult height increased by 4.3 cm in boys and 2.7 cm in girls between 1957 and 1977, the increment being less in the second decade than in the first. Sitting height showed practically no increase whatever; almost the whole secular trend was due to change in leg length. Japanese now have trunk/leg proportions much more similar to those of North Europeans than was the case 20 years ago, but their adult height remains about one standard deviation lower.

There is growing concern over the effects of sedentary lifestyles on the health of young people. Recent rapid increases in juvenile obesity have received a great deal of attention in the scientific and popular press and have been attributed partly to television viewing, computer games and other sedentary behaviours. These are thought to compete with physical activity. There is a 'moral panic' concerning the 'couch kids' culture in modern western society. Project STIL (Sedentary Teenagers and Inactive Lifestyles) at Loughborough University is investigating 'what young people do' and focuses on active and inactive pursuits chosen in their leisure time. The following issues are addressed in this paper with specific reference to young people: how do we define 'sedentary behaviour' and do key sedentary behaviours displace physical activity? Are key sedentary behaviours obesogenic? What are the secular trends for children and youth for TV viewing? Our results for young people suggest that: 1. TV viewing and video-game playing are largely uncorrelated with physical activity, suggesting that there is time for both 2. meta-analytic findings show that body fatness is not related in any clinically meaningful way with key sedentary behaviours 3. although more children and youth have greater access to TVs than in previous generations, the amount of TV watched per head has not changed for 40 years. Preliminary findings from Project STIL suggest that inactivity is more complex that we sometimes think. Indeed, measures of 'couch potato-ism', such as TV viewing, may be inappropriate markers of inactivity.

It has long been recognized that there are "critical periods" during mammalian development when exposure to specific environmental stimuli are required in order to elicit the normal development of particular anatomical structures or their normal functioning. The responses of the organism to these stimuli depend on a specific level of anatomical maturation and a state of rapid anatomical and/or functional change. This discussion of critical periods in growth is not confined to the classic definition of a narrow time frame of development during which a particular environmental threshold or limit must exist for normal growth and function to ensue. Using both auxological and epidemiological approaches, we suggest a lifespan perspective which encompasses accumulating and interacting risks that are manifest from prenatal life onward. By understanding the process of growth and development, and by scrutinizing the growth process, early variations that lead to later disease can be identified. Here we review a significant amount of the evidence that links exposure during growth to later morbidity and mortality.The fetus appears to respond to insults during the prenatal period through the process of "programming," which has short-term survival advantages but may have a longterm disadvantage in that it is associated with cardiovascular disease, hypertension, type II diabetes, and later obesity. Low birth weight combined with rapid postnatal growth during infancy also appears to be associated, for instance, with later childhood and adult sequelae in terms of glucose tolerance and obesity. Independent of birth weight, the timing of adiposity rebound during mid-childhood also predicts later obesity. The timing, magnitude, and duration of adolescent growth and maturation are associated with critical body composition changes, including the normal acquisition of body fat and bone mineralization. In particular, the acquisition of appropriate peak bone mass is critical in determining the later risk of osteoporosis.A putative causal mechanism linking early growth variation to later chronic disease risk through telomeric attrition is discussed. The obligatory loss of telomeric DNA with each cell division serves as a mitotic clock and marks the rate of growth and repair processes in the cell. Although much more work is required, existing studies support the notion that telomere shortening is not only a clock of cellular division, but also marks relative growth rate, as well as contributing to common degenerative processes of aging through its impact on cellular senescence. Yrbk Phys Anthropol 45: 159 -184, 2002.