Daily Papers

In this paper, we suggest a novel method for detecting mortality deceleration. We focus on the gamma-Gompertz frailty model and suggest the subtraction of a penalty in the log-likelihood function as an alternative to traditional likelihood inference and hypothesis testing. Over existing methods, our method offers advantages, such as avoiding the use of a p-value, hypothesis testing, and asymptotic distributions. We evaluate the performance of our approach by comparing it with traditional likelihood inference on both simulated and real mortality data. Results have shown that our approach is more accurate in detecting mortality deceleration and provides more reliable estimates of the underlying parameters. The proposed method is a significant contribution to the literature as it offers a powerful tool for analyzing mortality patterns.

Whether the risk of death keeps climbing at extreme ages or levels off has divided researchers for a century. We show this conflict reflects a moving target. Using cohort data from twelve low-mortality populations, we find that mortality deceleration and plateau onset shift steadily later across cohorts born from the mid-19th to the early-20th century. The data support a plateau across the full cohort range, though evidence weakens for the youngest, incompletely observed cohorts. In these younger cohorts, deceleration begins near age 100, and the fitted plateau begins beyond age 108. Because past studies focused on different cohorts and fixed age ranges, they sampled different phases of the exact same shift. The mortality plateau has no fixed age: it has been rescheduled.

This paper presents a novel approach for modeling mortality rates above age 70 by proposing a mixture-based model. This model is compared to four other widely used models: the Beard, Gompertz, Makeham, and Perks models. Our model can capture the complex behavior of mortality rates at all ages, providing a more accurate representation of the data. To evaluate the performance of our model, we applied it to two countries with different data quality: Japan and Brazil. Our results show that the proposed model outperforms the other models in both countries, particularly in Japan where it obtained an absolute mean percentage error of less than 7%, while the other models presented values greater than 30%. This highlights the ability of our model to adapt to different data quality and country-specific mortality patterns. In summary, this paper presents a mixture-based model that captures the behavior of mortality rates at all ages and outperforms other widely used models in both high- and low-quality data settings. This model can improve mortality prediction and inform public health policy.

Age-specific mortality improvements are non-uniform, neither across ages nor across time. We propose a two-step procedure to estimate the rates of mortality improvement (RMI) in age-specific death rates (ASDR) at ages 85 and above for ten European countries from 1950 to 2019. In the first step, we smooth the raw death counts and estimate ASDR using four different methods: one parametric (gamma-Gompertz-Makeham), two non-parametric (P-splines and PCLM), and a novel Bayesian procedure to handle fluctuations resulting from ages with zero death counts. We compare the goodness of fit of the four smoothing methods and calculate the year-to-year ASDR differences according to the best-fitting one. We fit a piecewise linear function to these differences in the second step. The slope in each linear segment captures the average RMI in the respective year range. For each age, we calculate the goodness of fit in the last linear segment to assess how informative the estimated RMI of current mortality change is. The estimated rates of mortality improvement or deterioration (RMI) can be used to make short-term social, health, and social planning, as well as more precise mortality forecasts.

A growing literature argues that progress in human longevity is slowing, and that this slowdown may signal an approaching biological limit to lifespan. The argument rests on visible flattening of cumulative life expectancy records, evaluated through linear regressions or through comparisons of average gains across decades. These summaries, however, provide only weak evidence for slowing improvements, because they cannot distinguish a true from an apparent slowdown. An apparent slowdown may arise due to periods of low variance around unchanged mean annual gains. Applying a Bayesian change-point framework to annual gains, both at the best-practice frontier and separately for each record-holding country, we find no evidence that the expected annual gain has changed across nearly two centuries, but strong evidence that its variance has moved through distinct historical regimes, with progress most regular in recent decades. The recent flattening is consistent with a low-variance regime and provides little evidence for a decline in the underlying mean pace of improvement. Claims that the best-practice frontier signals a biological ceiling should therefore not rest on the recent bend in the cumulative record alone. The frontier is better read as an empirical benchmark, the highest country-specific survival achieved under observed historical conditions.

Human aging is marked by a steady rise in the risk of dying with age-a process demographers call senescence. Over the past century, life expectancy has risen dramatically, but is this because we are aging slower, or simply starting it later? Vaupel hypothesizes that the pace at which individuals age may be constant, with gains in longevity coming from the delayed onset of senescence rather than its slowing down. We test this idea using a new framework that decomposes the pace of senescence into three components: a biological baseline, a long-term trend, and the cumulative impact of period shocks. Applying this to cohort mortality data above age 80 from 12 countries, we find that once period shocks are accounted for, there is no statistical evidence of a long-term trend, consistent with Vaupel's hypothesis. Analyses using lower starting ages yield the same qualitative conclusion. Rather than indicating a change in the process that drives senescence, these variations are consistent with echoes of shared historical events. These results suggest that while longevity has shifted, the rhythm of human aging may be conserved.

The Makeham term is a crucial element in mortality modeling, representing a constant additive hazard that addresses background mortality factors unrelated to aging. Widely used in mortality analysis, this term enables the capture of risks not linked to age-related decline. This paper aims to explore the relationship between Makeham mortality models and competing risk frameworks, investigating how Makeham models can be analyzed within the context of competing risks. It provides insights into the mathematical properties, interpretation, and applicability of Makeham models in modeling mortality risks associated with various causes of death. Additionally, it demonstrates that competing risk models can be represented as mixture models, enhancing understanding of mortality dynamics. The contribution lies in showing that Makeham mortality models, when represented as mixtures, offer a straightforward specification that can accommodate unobserved heterogeneity and distinguish between senescent and extrinsic mortality. By expressing Makeham models as a convex combination of probability distributions, the paper allows the estimation of premature mortality profiles, particularly at older ages, where most deaths are assumed to be senescent. It also facilitates the estimation of senescent mortality, which is crucial for studying the aging process.

\noindent The modal age at death is an increasingly used measure for understanding longevity and mortality patterns. However, existing estimation methods focus on point estimates, overlooking the inherent variability and uncertainty in mortality data. This study addresses this gap by introducing a probabilistic framework for estimating the probability distribution of the modal age at death. Using a multinomial model for age-specific death counts and leveraging a Gaussian approximation, our methodology captures variability while aligning with the discrete nature of mortality data. Empirical examples are based on mortality data from six different countries. By quantifying uncertainty around the modal age at death and improving robustness to data fluctuations, this approach offers valuable insights for demographic research and policy planning.

Automatic Adjustment Mechanisms (AAM) are legal instruments that help social security systems respond to demographic and economic changes. In Brazil, the Social Security Factor (SSF) was introduced in the late 1990s as an AAM to link retirement benefits to life expectancy at the retirement age, with the hope of promoting contributory justice and discouraging early retirement. Recent research has highlighted the limitations of right-censored life tables, such as those used in Brazil. It has recommended using the gamma-Gompertz-Makeham (GGM) model to estimate adult and old-age mortality. This study investigated the impact of right-censoring on the SSF by comparing the official SSF and other social security metrics with a counterfactual scenario computed based on fitted GGM models. The results indicate that from 2004 to 2012, official life tables may have negatively impacted retirees' income, particularly for those who delayed their retirement. Furthermore, the GGM-fitted models' life expectancies had more stable paths over time, which could have helped with long-term planning. This study's findings are significant for policymakers as they highlight the importance of using appropriate mortality metrics in AAMs to ensure accurate retirement benefit payments. They also underscore the need to consider the potential impacts of seemingly innocuous hypotheses on public action outcomes. Overall, this study provides valuable insights for public planners and policymakers looking to enhance the effectiveness and fairness of social security systems.

This work aims to understand how scaling improves language models, specifically in terms of training dynamics. We find that language models undergo loss deceleration early in training; an abrupt slowdown in the rate of loss improvement, resulting in piecewise linear behaviour of the loss curve in log-log space. Scaling up the model mitigates this transition by (1) decreasing the loss at which deceleration occurs, and (2) improving the log-log rate of loss improvement after deceleration. We attribute loss deceleration to a type of degenerate training dynamics we term zero-sum learning (ZSL). In ZSL, per-example gradients become systematically opposed, leading to destructive interference in per-example changes in loss. As a result, improving loss on one subset of examples degrades it on another, bottlenecking overall progress. Loss deceleration and ZSL provide new insights into the training dynamics underlying language model scaling laws, and could potentially be targeted directly to improve language models independent of scale. We make our code and artefacts available at: https://github.com/mirandrom/zsl

PURPOSE: Subarachnoid hemorrhage (SAH) entails high morbidity and mortality rates. Convolutional neural networks (CNN), a form of deep learning, are capable of generating highly accurate predictions from imaging data. Our objective was to predict mortality in SAH patients by processing the initial CT scan on a CNN based algorithm. METHODS: Retrospective multicentric study of a consecutive cohort of patients with SAH between 2011-2022. Demographic, clinical and radiological variables were analyzed. Pre-processed baseline CT scan images were used as the input for training a CNN using AUCMEDI Framework. Our model's architecture leverages the DenseNet-121 structure, employing transfer learning principles. The output variable was mortality in the first three months. Performance of the model was evaluated by statistical parameters conventionally used in studies involving artificial intelligence methods. RESULTS: Images from 219 patients were processed, 175 for training and validation of the CNN and 44 for its evaluation. 52%(115/219) of patients were female, and the median age was 58(SD=13.06) years. 18.5%(39/219) were idiopathic SAH. Mortality rate was 28.5%(63/219). The model showed good accuracy at predicting mortality in SAH patients exclusively using the images of the initial CT scan (Accuracy=74%, F1=75% and AUC=82%). CONCLUSION: Modern image processing techniques based on AI and CNN make possible to predict mortality in SAH patients with high accuracy using CT scan images as the only input. These models might be optimized by including more data and patients resulting in better training, development and performance on tasks which are beyond the skills of conventional clinical knowledge.