Research Paper Volume 8, Issue 3 pp 539—546

Figure 1. Three methods to examine the effects of caloric restriction and/or genetic disruption of growth hormone signaling on aging in mice. In Population A, caloric restriction entailed an intake of 30% less than the ad libitum dietary intake and growth hormone signaling was disrupted by knockout of the growth hormone receptor gene Ghr/Ghrbp [19]. In Population B, caloric restriction entailed an intake of 40% less than the ad libitum dietary intake and growth hormone signaling was disrupted by knockout of growth hormone-releasing hormone gene Ghrh [20]. (A, B) Age-dependent survival of the groups of mice in Population A (A) and Population B (B) depicted as Kaplan-Meier curves. These two figures have been published previously [19, 20] and are given here as references. The copyright of Figure 1A is with the National Academy of Sciences of the USA; the copyright of Figure 1B is with the authors of the original publication [20]. (C, D) Age-dependent mortality rates of the groups of mice in Population A (C) and Population B (D) given on a logarithmic scale. The mortality rates are expressed in deaths per 10,000 mice per day. The linear increase in mortality rate on a logarithmic scale is classically interpreted as an aging rate. (E, F) Age-dependent aging rates of the groups of mice in Population A (E) and Population B (F). Contrary to the aging rates estimated by the classical method in Table 2, these aging rates were calculated without modeling the age-dependent mortality rates, describe the increases in the mortality rates on a linear scale, and are dependent on age themselves. The aging rates are expressed in deaths per 10,000 mice per day per day, which equals the change in mortality rate per day.