Recent work shows that in complex model classes, interpolators can achieve statistical generalization and even be optimal for statistical learning. However, despite increasing interest in learning models with good causal properties, there is no understanding of whether such interpolators can also achieve . To address this gap, we study causal learning from observational data through the lens of interpolation and its counterpart---regularization. Under a simple linear causal model, we derive precise asymptotics for the causal risk of the min-norm interpolator and ridge regressors in the high-dimensional regime. We find a large range of behavior that can be precisely characterized by a new measure of . When confounding strength is positive, which holds under independent causal mechanisms---a standard assumption in causal learning---we find that interpolators cannot be optimal. Indeed, causal learning requires stronger regularization than statistical learning. Beyond this assumption, when confounding is negative, we observe a phenomenon of self-induced regularization due to positive alignment between statistical and causal signals. Here, causal learning requires weaker regularization than statistical learning, interpolators can be optimal, and optimal regularization can even be negative.

Learning about the causal structure of the world is a fundamental problem for human cognition. Causal models and especially causal learning have proved to be difficult for large pretrained models using standard techniques of deep learning. In contrast, cognitive scientists have applied advances in our formal understanding of causation in computer science, particularly within the Causal Bayes Net formalism, to understand human causal learning. In the very different tradition of reinforcement learning, researchers have described an intrinsic reward signal called "empowerment" which maximizes mutual information between actions and their outcomes. "Empowerment" may be an important bridge between classical Bayesian causal learning and reinforcement learning and may help to characterize causal learning in humans and enable it in machines. If an agent learns an accurate causal world model, they will necessarily increase their empowerment, and increasing empowerment will lead to a more accurate causal world model. Empowerment may also explain distinctive features of childrens causal learning, as well as providing a more tractable computational account of how that learning is possible. In an empirical study, we systematically test how children and adults use cues to empowerment to infer causal relations, and design effective causal interventions.

Recent work shows that in complex model classes, interpolators can achieve statistical generalization and even be optimal for statistical learning. However, despite increasing interest in learning models with good causal properties, there is no understanding of whether such interpolators can also achieve causal generalization. To address this gap, we study causal learning from observational data through the lens of interpolation and its counterpart---regularization. Under a simple linear causal model, we derive precise asymptotics for the causal risk of the min-norm interpolator and ridge regressors in the high-dimensional regime. We find a large range of behavior that can be precisely characterized by a new measure of confounding strength.

--In this work, we investigate causal learning of independent causal mechanisms from a Bayesian perspective. Confirming previous claims from the literature, we show in a didactically accessible manner that unlabeled data (i.e., cause realizations) do not improve the estimation of the parameters defining the mechanism. Furthermore, we observe the importance of choosing an appropriate prior for the cause and mechanism parameters, respectively. Specifically, we show that a factorized prior results in a factorized posterior, which resonates with Janz-ing and Sch olkopf's definition of independent causal mechanisms via the Kolmogorov complexity of the involved distributions and with the concept of parameter independence of Heckerman et al. Impact Statement --Learning the effect from a given cause is an important problem in many engineering disciplines, specifically in the field of surrogate modeling, which aims to reduce the computational cost of numerical simulations. Causal learning, however, cannot make use of unlabeled data - i.e., cause realizations - if the mechanism that produces the effect is independent from the cause. In this work, we recover this well-known fact from a Bayesian perspective.

True intelligence hinges on the ability to uncover and leverage hidden causal relations. Despite significant progress in AI and computer vision (CV), there remains a lack of benchmarks for assessing models' abilities to infer latent causality from complex visual data. In this paper, we introduce \textsc{\textbf{Causal3D}}, a novel and comprehensive benchmark that integrates structured data (tables) with corresponding visual representations (images) to evaluate causal reasoning. Designed within a systematic framework, Causal3D comprises 19 3D-scene datasets capturing diverse causal relations, views, and backgrounds, enabling evaluations across scenes of varying complexity. We assess multiple state-of-the-art methods, including classical causal discovery, causal representation learning, and large/vision-language models (LLMs/VLMs). Our experiments show that as causal structures grow more complex without prior knowledge, performance declines significantly, highlighting the challenges even advanced methods face in complex causal scenarios. Causal3D serves as a vital resource for advancing causal reasoning in CV and fostering trustworthy AI in critical domains.

Due to the challenge posed by multi-source and heterogeneous data collected from diverse environments, causal relationships among features can exhibit variations influenced by different time spans, regions, or strategies. This diversity makes a single causal model inadequate for accurately representing complex causal relationships in all observational data, a crucial consideration in causal learning. To address this challenge, the nonlinear Causal Kernel Clustering method is introduced for heterogeneous subgroup causal learning, highlighting variations in causal relationships across diverse subgroups. The main component for clustering heterogeneous subgroups lies in the construction of the $u$-centered sample mapping function with the property of unbiased estimation, which assesses the differences in potential nonlinear causal relationships in various samples and supported by causal identifiability theory. Experimental results indicate that the method performs well in identifying heterogeneous subgroups and enhancing causal learning, leading to a reduction in prediction error.

Recent work shows that in complex model classes, interpolators can achieve statistical generalization and even be optimal for statistical learning. However, despite increasing interest in learning models with good causal properties, there is no understanding of whether such interpolators can also achieve causal generalization. To address this gap, we study causal learning from observational data through the lens of interpolation and its counterpart---regularization. Under a simple linear causal model, we derive precise asymptotics for the causal risk of the min-norm interpolator and ridge regressors in the high-dimensional regime. We find a large range of behavior that can be precisely characterized by a new measure of confounding strength.

Causal learning is the cognitive process of developing the capability of making causal inferences based on available information, often guided by normative principles. This process is prone to errors and biases, such as the illusion of causality, in which people perceive a causal relationship between two variables despite lacking supporting evidence. This cognitive bias has been proposed to underlie many societal problems, including social prejudice, stereotype formation, misinformation, and superstitious thinking. In this research, we investigate whether large language models (LLMs) develop causal illusions, both in real-world and controlled laboratory contexts of causal learning and inference. To this end, we built a dataset of over 2K samples including purely correlational cases, situations with null contingency, and cases where temporal information excludes the possibility of causality by placing the potential effect before the cause. We then prompted the models to make statements or answer causal questions to evaluate their tendencies to infer causation erroneously in these structured settings. Our findings show a strong presence of causal illusion bias in LLMs. Specifically, in open-ended generation tasks involving spurious correlations, the models displayed bias at levels comparable to, or even lower than, those observed in similar studies on human subjects. However, when faced with null-contingency scenarios or temporal cues that negate causal relationships, where it was required to respond on a 0-100 scale, the models exhibited significantly higher bias. These findings suggest that the models have not uniformly, consistently, or reliably internalized the normative principles essential for accurate causal learning.

Understanding causal models is important in a number of fields, from healthcare to economics, as it allows for precise forecasting a training of reinforcement learning. Learning causal models involves extracting potential non-linear relationships and dependencies between variables from sampled time-series. For example, modelling of biomarkers of non-communicable disase as a function of diet and action monitoring has shown the potential of being a powerful tool to guide the recommendations on healthy diet. We aim to learn causal models that extend basic causal models in several directions, which are relevant in biomedical appliations. In particular, such causal models need to handle nonlinear causality, such as the competition among bacterial strains for metabolites. Likewise, one may consider constraints that become active beyond certain thresholds. Dealing with latent variables, such as hormone concentrations, is a challenge that demands a balance between model complexity and interpretability. These models should also consider cyclic relationships, time-series dynamics, and mixture-model aspects, accommodating individual variations in metabolism without predefined subgroups.