Life-history theory and climate change: resolving population and parental investment paradoxes

Population growth in the next half-century is on pace to raise global carbon emissions by half. Carbon emissions are associated with fertility as a by-product of somatic and parental investment, which is predicted to involve time orientation/preference as a mediating psychological mechanism. Here, we draw upon life-history theory (LHT) to investigate associations between future orientation and fertility, and their impacts on carbon emissions. We argue ' -strategy' life history (LH) in high-income countries has resulted in parental investment behaviours involving future orientation that, paradoxically, promote unsustainable carbon emissions, thereby lowering the Earth's or carrying capacity. Increasing the rate of approach towards this capacity are ' -strategy' LHs in low-income countries that promote population growth. We explore interactions between future orientation and development that might slow the rate of approach towards global . Examination of 67 000 individuals across 75 countries suggests that future orientation interacts with the relationship between environmental risk and fertility and with development related parental investment, particularly investment in higher education, to slow population growth and mitigate carbon emissions. Results emphasize that LHT will be an important tool in understanding the demographic and consumption patterns that drive anthropogenic climate change

RECOMBINANT HUMAN INTERLEUKIN-1 RECEPTOR ANTAGONIST IN THE TREATMENT OF PATIENTS WITH SEPSIS SYNDROME - RESULTS FROM A RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED TRIAL

Objective.-To further define the safety and efficacy of recombinant human interleukin 1 receptor antagonist (rhlL-1ra) in the treatment of sepsis syndrome. Study Design.-Randomized, double-blind, placebo-controlled, multicenter, multinational clinical trial. Population.-A total of 893 patients with sepsis syndrome received an intravenous loading dose of rhIL-1ra, 100 mg, or placebo followed by a continuous 72-hour intravenous infusion of rhIL-1ra (1.0 or 2.0 mg/kg per hour) or placebo. Outcome Measure.-Twenty-eight-day all-cause mortality. Results.-There was not a significant increase in survival time for rhIL-1ra treatment compared with placebo among all patients who received the study medication (n=893; generalized Wilcoxon statistic, P=.22) or among patients with shock at study entry (n=713; generalized Wilcoxon statistic, P=.23), the two primary efficacy analyses specified a priori for this trial. Results from secondary analyses suggest an increase in survival time with rhIL-1ra treatment among patients with dysfunction of one or more organs (n=563; linear dose-response, P=.009). Retrospective analysis demonstrated an increase In survival time with rhIL-1ra treatment among patients with a predicted risk of mortality of 24% or greater (n=580; linear dose-response, P=.005) as well as among patients with both dysfunction of one or more organs and a predicted risk of mortality of 24% or greater (n=411; linear dose-response, P=.002). Conclusions.-There was not a statistically significant increase in survival time for rhIL-1ra treatment compared with placebo among all patients who received the study medication or among patients with shock at study entry. Secondary and retrospective analyses of efficacy suggest that treatment with rhIL-1ra results in a dose-related increase in survival time among patients with sepsis who have organ dysfunction and/or a predicted risk of mortality of 24% or greate