Four species of grass generate half of all human-consumed calories. However, abundant biological data on species that produce our food remain largely inaccessible, imposing direct barriers to understanding crop yield and fitness traits. Here, we assemble and analyse a continent-wide database of field experiments spanning 10 years and hundreds of thousands of machine-phenotyped populations of ten major crop species. Training an ensemble of machine learning models, using thousands of variables capturing weather, ground sensor, soil, chemical and fertilizer dosage, management and satellite data, produces robust cross-continent yield models exceeding R² = 0.8 prediction accuracy. In contrast to ‘black box’ analytics, detailed interrogation of these models reveals drivers of crop behaviour and complex interactions predicting yield and agronomic traits. These results demonstrate the capacity of machine learning models to interrogate large datasets, generate new and testable outputs and predict crop behaviour, highlighting the powerful role of data in the future of food.

Several organisms, including humans, display a deceleration in mortality rates at advanced ages. This mortality deceleration is sufficiently rapid to allow late-life mortality to plateau in old age in several species, causing the apparent cessation of biological ageing. Here, it is shown that late-life mortality deceleration (LLMD) and late-life plateaus are caused by common demographic errors. Age estimation and cohort blending errors introduced at rates below 1 in 10,000 are sufficient to cause LLMD and plateaus. In humans, observed error rates of birth and death registration predict the magnitude of LLMD. Correction for these sources of demographic error using a mixed linear model eliminates LLMD and late-life mortality plateaus (LLMPs) without recourse to biological or evolutionary models. These results suggest models developed to explain LLMD have been fitted to an error distribution, that ageing does not slow or stop during old age in humans, and that there is a finite limit to human longevity. In diverse species, mortality rates increase with age at a relatively fixed rate within populations. However, recent discoveries have suggested this relationship breaks down in advanced old age, with mortality rate increases slowing and even reaching a plateau. This late-life mortality deceleration has initiated sustained debate on the cause of late-life deceleration and plateaus. Proposed explanations include evolutionary patterns, the exhaustion of selective pressure, population heterogeneity, and even the cessation of the ageing process. Here, I demonstrate that apparent late-life mortality decelerations and plateaus can be generated by low-frequency errors. I then reveal how indicators of demographic data quality predict the magnitude of late-life mortality deceleration and the existence of late-life plateaus in human populations. These findings suggest that human late-life mortality plateaus are largely, if not entirely, artefacts of error processes. As a result, late-life mortality plateaus and decelerations may be explained by error patterns in humans and many other species without invoking complex biological, heterogeneity, or evolutionary models. This finding has immediate consequences for demographic modelling, evolutionary biology, and the projected upper limits of human and nonhuman life.

Genetic factors are strongly implicated in the susceptibility to develop externalizing syndromes such as attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder, conduct disorder, and substance use disorder (SUD). Variants in the ADGRL3 (LPHN3) gene predispose to ADHD and predict ADHD severity, disruptive behaviors comorbidity, long-term outcome, and response to treatment. In this study, we investigated whether variants within ADGRL3 are associated with SUD, a disorder that is frequently co-morbid with ADHD. Using family-based, case-control, and longitudinal samples from disparate regions of the world (n = 2698), recruited either for clinical, genetic epidemiological or pharmacogenomic studies of ADHD, we assembled recursive-partitioning frameworks (classification tree analyses) with clinical, demographic, and ADGRL3 genetic information to predict SUD susceptibility. Our results indicate that SUD can be efficiently and robustly predicted in ADHD participants. The genetic models used remained highly efficient in predicting SUD in a large sample of individuals with severe SUD from a psychiatric institution that were not ascertained on the basis of ADHD diagnosis, thus identifying ADGRL3 as a risk gene for SUD. Recursive-partitioning analyses revealed that rs4860437 was the predominant predictive variant. This new methodological approach offers novel insights into higher order predictive interactions and offers a unique opportunity for translational application in the clinical assessment of patients at high risk for SUD.

The observation of individuals attaining remarkable ages, and their concentration into geographic sub-regions or ‘blue zones’, has generated considerable scientific interest. Proposed drivers of remarkable longevity include high vegetable intake, strong social connections, and genetic markers. Here, we reveal new predictors of remarkable longevity and ‘supercentenarian’ status. In the United States, supercentenarian status is predicted by the absence of vital registration. The state-specific introduction of birth certificates is associated with a 69-82% fall in the number of supercentenarian records. In Italy, England, and France, which have more uniform vital registration, remarkable longevity is instead predicted by poverty, low per capita incomes, shorter life expectancy, higher crime rates, worse health, higher deprivation, fewer 90+ year olds, and residence in remote, overseas, and colonial territories. In England and France, higher old-age poverty rates alone predict more than half of the regional variation in attaining a remarkable age. Only 18% of ‘exhaustively’ validated supercentenarians have a birth certificate, falling to zero percent in the USA, and supercentenarian birthdates are concentrated on days divisible by five: a pattern indicative of widespread fraud and error. Finally, the designated ‘blue zones’ of Sardinia, Okinawa, and Ikaria corresponded to regions with low incomes, low literacy, high crime rate and short life expectancy relative to their national average. As such, relative poverty and short lifespan constitute unexpected predictors of centenarian and supercentenarian status and support a primary role of fraud and error in generating remarkable human age records.