Complex systems can be described at myriad different scales, and their causal workings often have a multiscale structure (e.g., a computer can be described at the microscale of its hardware circuitry, the mesoscale of its machine code, and the macroscale of its operating system). While scientists study and model systems across the full hierarchy of their scales, from microphysics to macroeconomics, there is debate about what the macroscales of systems can possibly add beyond mere compression. To resolve this long-standing issue, here, a new theory of emergence is introduced that can distinguish which scales irreducibly contribute to a system’s causal workings. The theory’s application is demonstrated in coarse grains of Markov chains, revealing a novel measure of emergent complexity: how widely distributed a system’s causal contributions are across its hierarchy of scales.

Complex systems can be described at myriad different scales, and their causal workings often have multiscale structure (e.g., a computer can be described at the microscale of its hardware circuitry, the mesoscale of its machine code, and the macroscale of its operating system). While scientists study and model systems across the full hierarchy of their scales, from microphysics to macroeconomics, there is debate about what the macroscales of systems can possibly add beyond mere compression. To resolve this longstanding issue, here a new theory of emergence is introduced wherein the different scales of a system are treated like slices of a higher-dimensional object. The theory can distinguish which of these scales possess unique causal contributions, and which are not causally relevant. Constructed from an axiomatic notion of causation, the theory's application is demonstrated in coarse-grains of Markov chains. It identifies all cases of macroscale causation: instances where reduction to a microscale is possible, yet lossy about causation. Furthermore, the theory posits a causal apportioning schema that calculates the causal contribution of each scale, showing what each uniquely adds. Finally, it reveals a novel measure of emergent complexity: how widely distributed a system's causal workings are across its hierarchy of scales.

The requirements for a falsifiable and non-trivial theory of consciousness significantly constrain such theories. Specifically, recent research on the Unfolding Argument and the Substitution Argument has given us formal tools to analyze requirements for a theory of consciousness. I show via a new Proximity Argument that these requirements especially constrain the potential consciousness of contemporary Large Language Models (LLMs) because of their proximity to systems that are equivalent to LLMs in terms of input/output function; yet, for these functionally equivalent systems, there cannot be any non-trivial theory of consciousness that judges them conscious. This forms the basis of a disproof of contemporary LLM consciousness. I then show a positive result, which is that theories of consciousness based on (or requiring) continual learning do satisfy the stringent formal constraints for a theory of consciousness in humans. Intriguingly, this work supports a hypothesis: If continual learning is linked to consciousness in humans, the current limitations of LLMs (which do not continually learn) are intimately tied to their lack of consciousness.

One of the reasons complex systems are complex is because they have multiscale structure. How does this multiscale structure come about? We argue that it reflects an emergent hierarchy of scales that contribute to the system's causal workings. An example is how a computer can be described at the level of its hardware circuitry but also its software. But we show that many systems, even simple ones, have such an emergent hierarchy, built from a small subset of all their possible scales of description. Formally, we extend the theory of causal emergence (2.0) so as to analyze the causal contributions across the full multiscale structure of a system rather than just over a single path that traverses the system's scales. Our methods reveal that systems can be classified as being causally top-heavy or bottom-heavy, or their emergent hierarchies can be highly complex. We argue that this provides a more specific notion of scale-freeness (here, when causation is spread equally across the scales of a system) than the standard network science terminology. More broadly, we provide the mathematical tools to quantify this complexity and provide diverse examples of the taxonomy of emergent hierarchies. Finally, we demonstrate the ability to engineer not just degree of emergence in a system, but how that emergence is distributed across the multiscale structure.

Causation is fundamentally important to science, and yet our understanding of causation is spread out across disparate fields, with different measures of causation having been proposed in philosophy, statistics, psychology, and other areas. Here we examined over a dozen popular measures of causation, all independently developed and widely used, originating in different fields. We identify a high degree of consilience, in that measures are often very similar, or indeed often rediscovered. This is because, we show, measures of causation are based on a small set of related “causal primitives”: sufficiency and necessity, or alternatively, determinism and degeneracy. These primitives are ways of capturing the degree of uncertainty inherent in causal relationships. In turn, these results help us understand the phenomenon whereby macroscales can reduce the uncertainty in causal relationships, leading to stronger causes at macroscales—an outcome known as “causal emergence”. First identified using the effective information and later the integrated information in model systems, causal emergence has been found in real data across the sciences since. But is it simply a quirk of these original measures? Using a simple model system, we demonstrate how the consilience of causation guarantees that causal emergence is commonly found in causal measures, identifying instances across all measures analyzed. This finding sets the mathematical understanding of emergence on firmer ground, opening the door for the detection of natural scales of causal interaction in complex systems, as well as assisting with scientific modeling and experimental interventions.

Integrated information theory (IIT) starts from consciousness, which is subjective, and accounts for its presence and quality in objective, testable terms. Attempts to label as ‘pseudoscientific’ a theory distinguished by decades of conceptual, mathematical, and empirical developments expose a crisis in the dominant computational-functionalist paradigm, which is challenged by IIT’s consciousness-first paradigm.

This essay argues that neuroscience remains pre-paradigmatic in the Kuhnian sense, lacking a unifying theoretical framework despite impressive methodological advances. The author contends that consciousness is the missing organising principle, analogous to evolution in biology. Drawing on evidence of reproducibility failures in neuroimaging and the field's reliance on 'cool' rather than fundamental findings, the piece calls for placing consciousness at the centre of neuroscience.

Is reduction always a good scientific strategy? The existence of the special sciences above physics suggests not. Previous research has shown that dimensionality reduction (macroscales) can increase the dependency between elements of a system (a phenomenon called ‘causal emergence’). Here, we provide an umbrella mathematical framework for emergence based on information conversion. We show evidence that coarse-graining can convert information from one ‘type’ to another. We demonstrate this using the well-understood mutual information measure applied to Boolean networks. Using partial information decomposition, the mutual information can be decomposed into redundant, unique and synergistic information atoms. Then by introducing a novel measure of the synergy bias of a given decomposition, we are able to show that the synergy component of a Boolean network’s mutual information can increase at macroscales. This can occur even when there is no difference in the total mutual information between a macroscale and its underlying microscale, proving information conversion. We relate this broad framework to previous work, compare it to other theories, and argue it complexifies any notion of universal reduction in the sciences, since such reduction would likely lead to a loss of synergistic information in scientific models. This article is part of the theme issue ‘Emergent phenomena in complex physical and socio-technical systems: from cells to societies’.

Causal emergence is the theory that macroscales can reduce the noise in causal relationships, leading to stronger causes at the macroscale. First identified using the effective information and later the integrated information in model systems, causal emergence has been analyzed in real data across the sciences since. But is it simply a quirk of these original measures? To answer this question we examined over a dozen popular measures of causation, all independently developed and widely used, and spanning different fields from philosophy to statistics to psychology to genetics. All showed cases of causal emergence. This is because, we prove, measures of causation are based on a small set of related "causal primitives." This consilience of independently-developed measures of causation shows that macroscale causation is a general fact about causal relationships, is scientifically detectable, and is not a quirk of any particular measure of causation. This finding sets the science of emergence on firmer ground, opening the door for the detection of intrinsic scales of function in complex systems, as well as assisting with scientific modeling and experimental interventions.

The search for a scientific theory of consciousness should result in theories that are falsifiable. However, here we show that falsification is especially problematic for theories of consciousness. We formally describe the standard experimental setup for testing these theories. Based on a theory's application to some physical system, such as the brain, testing requires comparing a theory's predicted experience (given some internal observables of the system like brain imaging data) with an inferred experience (using report or behavior). If there is a mismatch between inference and prediction, a theory is falsified. We show that if inference and prediction are independent, it follows that any minimally informative theory of consciousness is automatically falsified. This is deeply problematic since the field's reliance on report or behavior to infer conscious experiences implies such independence, so this fragility affects many contemporary theories of consciousness. Furthermore, we show that if inference and prediction are strictly dependent, it follows that a theory is unfalsifiable. This affects theories which claim consciousness to be determined by report or behavior. Finally, we explore possible ways out of this dilemma.

This primer sets out causal emergence: cases where macro-level modelling exhibits greater causal efficacy than micro-descriptions. It introduces effective information as a measure, shows how coarse-graining and intervention guide model selection across scales, and addresses common misunderstandings. Framed as a reply to criticism, it situates causal emergence within debates on reductionism and multiscale explanation, offering concrete examples and practical notes for applying the framework to complex systems and observed behaviour.

Understanding of the evolved biological function of sleep has advanced considerably in the past decade. However, no equivalent understanding of dreams has emerged. Contemporary neuroscientific theories generally view dreams as epiphenomena, and the few proposals for their biological function are contradicted by the phenomenology of dreams themselves. Now, the recent advent of deep neural networks (DNNs) has finally provided the novel conceptual framework within which to understand the evolved function of dreams. Notably, all DNNs face the issue of overfitting as they learn, which is when performance on one data set increases but the network's performance fails to generalize (often measured by the divergence of performance on training vs. testing data sets). This ubiquitous problem in DNNs is often solved by modelers via "noise injections" in the form of noisy or corrupted inputs. The goal of this paper is to argue that the brain faces a similar challenge of overfitting, and that nightly dreams evolved to combat the brain's overfitting during its daily learning. That is, dreams are a biological mechanism for increasing generalizability via the creation of corrupted sensory inputs from stochastic activity across the hierarchy of neural structures. Sleep loss, specifically dream loss, leads to an overfitted brain that can still memorize and learn but fails to generalize appropriately. Herein this "overfitted brain hypothesis" is explicitly developed and then compared and contrasted with existing contemporary neuroscientific theories of dreams. Existing evidence for the hypothesis is surveyed within both neuroscience and deep learning, and a set of testable predictions are put forward that can be pursued both in vivo and in silico.

Gene regulatory networks (GRNs) process important information in developmental biology and biomedicine. A key knowledge gap concerns how their responses change over time. Hypothesizing long-term changes of dynamics induced by transient prior events, we created a computational framework for defining and identifying diverse types of memory in candidate GRNs. We show that GRNs from a wide range of model systems are predicted to possess several types of memory, including Pavlovian conditioning. Associative memory offers an alternative strategy for the biomedical use of powerful drugs with undesirable side effects, and a novel approach to understanding the variability and time-dependent changes of drug action. We find evidence of natural selection favoring GRN memory. Vertebrate GRNs overall exhibit more memory than invertebrate GRNs, and memory is most prevalent in differentiated metazoan cell networks compared with undifferentiated cells. Timed stimuli are a powerful alternative for biomedical control of complex in vivo dynamics without genomic editing or transgenes.

The internal workings of biological systems are notoriously difficult to understand. Due to the prevalence of noise and degeneracy in evolved systems, in many cases the workings of everything from gene regulatory networks to protein-protein interactome networks remain black boxes. One consequence of this black-box nature is that it is unclear at which scale to analyze biological systems to best understand their function. We analyzed the protein interactomes of over 1800 species, containing in total 8 782 166 protein-protein interactions, at different scales. We show the emergence of higher order 'macroscales' in these interactomes and that these biological macroscales are associated with lower noise and degeneracy and therefore lower uncertainty. Moreover, the nodes in the interactomes that make up the macroscale are more resilient compared with nodes that do not participate in the macroscale. These effects are more pronounced in interactomes of eukaryota, as compared with prokaryota; these results hold even after sensitivity tests where we recalculate the emergent macroscales under network simulations where we add different edge weights to the interactomes. This points to plausible evolutionary adaptation for macroscales: biological networks evolve informative macroscales to gain benefits of both being uncertain at lower scales to boost their resilience, and also being 'certain' at higher scales to increase their effectiveness at information transmission. Our work explains some of the difficulty in understanding the workings of biological networks, since they are often most informative at a hidden higher scale, and demonstrates the tools to make these informative higher scales explicit.

The internal workings of biological systems are notoriously difficult to understand. Due to the prevalence of noise and degeneracy in evolved systems, in many cases the workings of everything from gene regulatory networks to protein-protein interactome networks remain black boxes. One consequence of this black-box nature is that it is unclear at which scale to analyze biological systems to best understand their function. We analyzed the protein interactomes of over 1800 species, containing in total 8,782,166 protein-protein interactions, at different scales. We demonstrate the emergence of higher order ‘macroscales’ in these interactomes and that these biological macroscales are associated with lower noise and degeneracy and therefore lower uncertainty. Moreover, the nodes in the interactomes that make up the macroscale are more resilient compared to nodes that do not participate in the macroscale. These effects are more pronounced in interactomes of Eukaryota, as compared to Prokaryota. This points to plausible evolutionary adaptation for macroscales: biological networks evolve informative macroscales to gain benefits of both being uncertain at lower scales to boost their resilience, and also being ‘certain’ at higher scales to increase their effectiveness at information transmission. Our work explains some of the difficulty in understanding the workings of biological networks, since they are often most informative at a hidden higher scale, and demonstrates the tools to make these informative higher scales explicit.

ABSTRACT The biological sciences span many spatial and temporal scales in attempts to understand the function and evolution of complex systems-level processes, such as embryogenesis. It is generally assumed that the most effective description of these processes is in terms of molecular interactions. However, recent developments in information theory and causal analysis now allow for the quantitative resolution of this question. In some cases, macro-scale models can minimize noise and increase the amount of information an experimenter or modeler has about "what does what." This result has numerous implications for evolution, pattern regulation, and biomedical strategies. Here, we provide an introduction to these quantitative techniques, and use them to show how informative macro-scales are common across biology. Our goal is to give biologists the tools to identify the maximally-informative scale at which to model, experiment on, predict, control, and understand complex biological systems.

The fictions we conjure while we sleep may do something far more profound than reinforcing learning, says neuroscientist Erik Hoel

Information geometry has offered a way to formally study the efficacy of scientific models by quantifying the impact of model parameters on the predicted effects. However, there has been little formal investigation of causation in this framework, despite causal models being a fundamental part of science and explanation. Here, we introduce causal geometry, which formalizes not only how outcomes are impacted by parameters, but also how the parameters of a model can be intervened upon. Therefore, we introduce a geometric version of "effective information"-a known measure of the informativeness of a causal relationship. We show that it is given by the matching between the space of effects and the space of interventions, in the form of their geometric congruence. Therefore, given a fixed intervention capability, an effective causal model is one that is well matched to those interventions. This is a consequence of "causal emergence," wherein macroscopic causal relationships may carry more information than "fundamental" microscopic ones. We thus argue that a coarse-grained model may, paradoxically, be more informative than the microscopic one, especially when it better matches the scale of accessible interventions-as we illustrate on toy examples.

The connectivity of a network contains information about the relationships between nodes, which can denote interactions, associations, or dependencies. We show that this information can be analyzed by measuring the uncertainty (and certainty) contained in paths along nodes and links in a network. Specifically, we derive from first principles a measure known as effective information and describe its behavior in common network models. Networks with higher effective information contain more information in the relationships between nodes. We show how subgraphs of nodes can be grouped into macronodes, reducing the size of a network while increasing its effective information (a phenomenon known as causal emergence). We find that informative higher scales are common in simulated and real networks across biological, social, informational, and technological domains. These results show that the emergence of higher scales in networks can be directly assessed and that these higher scales offer a way to create certainty out of uncertainty.