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Age related macular degeneration (AMD) represent one of the first clinical entities that were correlated with ocular rigidity (OR). Measurements performed with both indirect and direct methodology have created some evidence that could support an etiopathogenic relation between OR and AMD. Our group has contributed to these data with measurements performed in living human eyes using a direct manometric methodology. However, since there is always the possibility that increased scleral rigidity is an epiphenomenon of AMD and not an etiologic factor, future work focusing on imaging, ocular hemodynamic evaluation and non-invasive rigidity recording could help clarify the possible role of sclera and choroidal vasculature in AMD and possibly provide novel means for intervening in pathophysiology of the disease.

Both epidemiological and clinical studies support an association between infections and autoimmune diseases with mental disorders. It has been suggested that infections and autoimmune diseases can increase the risk of mental disorders by inducing neuroinflammation potentially through immunopathological mechanisms. These mechanisms might increase the permeability of the blood–brain barrier leaving the brain more vulnerable to circulating brain-reactive autoantibodies and other immune components which can cause psychiatric symptoms. However, the association between infections and autoimmune diseases with mental disorders has rather consistently been shown to be bidirectional indicating that some of the associations could be partly explained by confounding factors as BMI and smoking. Nonetheless, dose–response associations have been found for autoimmune diseases and particularly for infections regarding the risk of development of mental disorders, and risks of mental disorders are further increased with the temporal proximity of the diagnosis, and if causal, it could show to be important risk factors for mental disorders. Future longitudinal studies are needed with measurements from multiple biological samples, ranging from material close to the brain, as cerebrospinal fluid (CSF), to analysis of blood, in order to clarify if the association between infections and autoimmune disorders and mental disorders is causal or rather an epiphenomenon. Nonetheless, screening for general medical conditions and particularly infections and autoimmune diseases in patients with onset of severe mental disorders, preferably based on CSF in combination with serum, is a key in order to improve the health condition of individuals with mental disorders. Continued research in the field is important since an increased understanding of the etiology of mental disorders can prompt a range of new treatment options in psychiatry.

The hypothesis that reactive oxygen species (ROS) can be not just associated with but causally implicated in disease was first made in 1956, but so far, the oxidative stress theory of disease has not led to major therapeutic breakthrough, and the use of antioxidant is now confined to the field of complementary medicine. This chapter reviews the lack of high-level clinical evidence for the effectiveness of antioxidants in preventing disease and the epistemological problems of the oxidative stress theory of disease. We conclude on possible ways forward to test this hypothesis with approaches that take into account personalized medicine. The previous oxidative stress model has helped neither to diagnose nor to treat possibly ROS-related or ROS-dependent diseases. The redox balance concept that low ROS levels are beneficial or tolerable and high levels are disease triggers and best reduced is apparently wrong. Physiological ROS signalling may become dysfunctional or a disease trigger by at least five mechanisms: a physiological source may appear at an unphysiological site, a physiological source may be underactivated (less common) or overactivated (more common), a new source may appear, a physiological source may be overactivated or underactivated, and a toxifying enzyme may convert an ROS signal molecule into a more reactive molecule. The latter three mechanisms may reach a physiological or nonphysiological target. All of these dysregulations may be the direct and essential cause of a disease (rarely the case) or just a secondary epiphenomenon, which will disappear once the non-ROS-related cause of the disease is cured (much more common). Importantly, these mechanisms are the same for almost every signalling system. Causal target validation (sources, toxifiers and targets) is essential in order to identify effective drugs and therapies for ROSopathies.

The aging of our society is a well known epiphenomenon. Yet the multiple consequences and impact on the travel and tourism industry are only starting to surface. Accustomed to dealing with the Silent Generation of the elderly, we investigate what characteristics the next wave of over 65’s will bring with it: their travelling patterns, their attitudes and their spending power. Surprising facts and features emerge.

In this chapter, we present and discuss two opposing views of linguistic meaning. The first view, which we call the view of meaning as something, maintains that there is such a thing as meaning. The second, which we call the view of meaning as nothing, maintains that there is no such a thing as meaning; meaning is the epiphenomenon of something more concrete and fundamental. As a prototypical incarnation of the view of meaning as something, we present the theory of meaning as reference, which draws a distinction between the linguistic expressions a language is made of and the object these expressions refer to. As an example of the view of meaning as nothing, we discuss the structuralist approach to meaning, whereby meaning is an emergent property of the system of grammatical relations that constitute a language. We conclude with a discussion of the strength and shortcomings of the two views and a curious parallel with cinematography.

In our own biology, in our very own body, we have been given the seeds of spirituality. I argue that life events and other experiences that activate particular biological mechanisms in our bodies have a spiritual meaning in themselves. Their spiritual dimension should not be understood as an epiphenomenon: it is fundamental and inescapably intertwined with its biological extent. The scope of self-transcendent experiences considered ranges from flow to mystical experiences. The biological mechanisms that seem to be involved focus on oxytocin cascades, which are an integral part of the regulation of social behaviour across mammal species. Oxytocin has been linked to feelings of love and connectedness as well as to faith. Interestingly, the moment where its concentration is at its highest is during childbirth. This article explores the different varieties of transcendent experience in relation to their biological support processes and the life events they accompany. It stresses the dangers of reducing biology to commodified processes that disregard the importance of their spiritual component. Showing respect to our physical experiences means acknowledging our own transcendence. If we fail doing so, we risk losing one of the most precious gifts we have received: the transcendent within.

Universities still give greater credence to the disciplinary specialist and do not yet fully appreciate the broader skill sets that individual interdisciplinarians have to offer. At the same time, research funders are not sufficiently aware of the potential unintended consequences for academic careers of their focus on funding for interdisciplinary research. Addressing these misalignments requires a shift from thinking of interdisciplinarity as an epiphenomenon to a more systemic, embedded approach. This necessitates a rebalancing or recalibration within our institutions and this chapter concludes with some suggestions for practical steps to secure greater consistency and coherence within the governance of interdisciplinarity.

As a reaction to Putnam’s multiple-realization argument, several philosophers have attempted to develop non-reductive physicalist theories in which the mental supervenes on its physical basis. Putnam himself presents a functionalist interpretation of the mind analogous to the functions of the software in a computer. The problem with functionalism in this version is that it presupposes that it is possible to simulate the mind regardless of whether it is a biological or non-biological matter upon which the functional “software” [or algorithm] is implemented. Another non-reductive theory regards the mental to emerge from the mechanisms operating in the brain. Seeing the mental as “emergent” from the physical not only implies different levels of reality, just like functionalism, but also allows the possibility of “downwards” causation in which events on the mental level may actively cause what happens on the physical level. Alternatively, to deny such a possibility makes the mental become a causally impotent epiphenomenon. The chapter concludes by rejecting the vertical perspective on the relation between the mental and the physical, which this debate presupposes.

The nature of consciousness remains one of the main unsolved questions in neurobiology. Although recent advances suggest that sooner or later we will be able to understand the neural mechanisms underlying awareness, it seems very difficult to understand how neural activity becomes a subjective experience, the so-called hard-problem of consciousness. The apparent intractable nature of this problem causes some scientists to avoid it altogether and deal only with the neural correlates of consciousness. However, for others, consciousness is an epiphenomenon, that is, something without a direct function, like the redness of blood – a characteristic which was not selected for, but was a consequence of the mechanism selected to deliver oxygen. In that view, qualia, the phenomenological experiences, correspond to internal discriminations that are reliable correlates of underlying neural mechanisms. Consciousness itself is not causal. It is the neural structures underlying conscious experience that are causal. In contrast, a hypothesis is proposed here for which the functional integration of cortical circuits could generate the conscious experience as a feedback mechanism that allows the brain to continuously alter its ongoing operation in order to get a very precise adjustment of the organism to its internal and external environment. This means that without consciousness the brain function would lose versatility and effectiveness.

Two hypotheses dominate the literature on systems consolidation of episodic memory: the transfer hypothesis and the transformation hypothesis. The former postulates a transfer of episodic memory from a fast-learning hippocampus to a slow-learning neocortex. The latter postulates that only the hippocampus genuinely stores episodic memories, and that systems consolidation arises due to multiple memory traces in the hippocampus and a transformation of episodic into semantic memories. While both hypotheses are supported by some evidence, they are contradicted by other, and hence remain controversial. Here, I suggest a new account of systems consolidation. It is based on the transformation hypothesis and introduces two modifications. First, episodic and semantic memory differ in their representational format, which is optimized for different purposes: Rigid sequences for episodic memories and flexible representations for semantic memory. Second, multiple memory traces in the hippocampus are not required to account for the temporal gradient of retrograde amnesia, if there is any. To this end, slow semantic learning from episodic memories suffices. The main hypothesis that I propose in this chapter is that systems consolidation is an epiphenomenon of semantic learning from episodic memory.

Continuous electroencephalography (cEEG) is an important diagnostic tool, frequently used to assess brain function and detect nonconvulsive seizures (NCS). The expansion of cEEG monitoring has led to the realization that rhythmic and periodic patterns are commonly seen in critically ill patients. Unfortunately, the significance and implications of many of these patterns remain poorly defined, making it difficult for the electroencephalographer to clearly communicate their meaning to the clinical team. For some of these patterns, there has been an association with increased risk of seizures and morbidity [1–4]. However, decision regarding if and how aggressively to treat these patterns remains controversial. Furthermore, the distinction between ictal and interictal can become blurred, making this decision even more challenging. Debate continues about whether these patterns intrinsically have potential for neuronal injury or whether they exist as an epiphenomenon of acute brain injury or encephalopathy [5]. A helpful conceptualization is to consider that each of these patterns lie on an ictal-interictal continuum (IIC), implying varying degrees of cortical irritability and need for treatment [6].

Once thought as the mere epiphenomenon of a largely unknown inflammatory process, Anti-Neutrophil Cytoplasmic Antibodies (ANCA) have gained growing attention in recent years as key players in the pathogenesis of small vessel inflammation. Genetic studies as well as animal and in vitro models suggest that multiple factors induce the generation of ANCA, which in turn have the ability to promote neutrophil activation and progression towards neutrophil extracellular trap (NET) development. A vicious circle emerges as NETs endowed with ANCA targets promote ANCA generation. Besides consolidated pathogenic data, less is yet known about the precise role of ANCA in the clinical practice.

The word consciousness is, if anything, even more ambiguous than habit and more or less closely allied terms or expressions (e.g., disposition, practice, routine, ritual, convention, and pattern of action). The pragmatist consensus regarding habit change (and it is the change of habits, not simply habits, that is at the center of this consensus) encompasses an account of consciousness or awareness in one or more of its most central senses. According to the pragmatists, the arrest of habits intensifies or heightens awareness; and such an alteration of consciousness aids agents in exercising control over both environing circumstances and their somatically rooted habits. That is, consciousness is not a mere epiphenomenon: “it seems to me,” Peirce claims, “that it exercises a real function in self-control” (c. 1906, CP 5.493). In addition to the intimate connection between arrested action and heightened awareness, however, we must also consider the integration of habits and the emergent, precarious, and yet quite effective form of autonomy characteristic of human agents. While the consensus in question involves a shift in perspective, one from consciousness to habituation and hence the alteration of habits, it does not simply jettison the concept of consciousness. It rather tries to explain consciousness in reference to the operation, dissolution, and modification of habits.

Time has a highly unstable place between the objective and the subjective. On the one side, there are very well known philosophical arguments trying to show that time has only a subjective reality, even that it is merely a subjective epiphenomenon. On the other side, we are compelled to take points of view as non dispensable elements of reality, at least of a reality capable of containing beings like us. And points of view offer a world of temporal entities existing in an objective way. Moreover, points of view themselves appear to be temporal entities among other temporal entities. We analyse both aspects of time. Our main focus will be McTaggart’s arguments against the reality of a fluent time, what he called temporal series of kind A. We will distinguish three very different arguments in McTaggart works. We analyse them in detail. And we reject their conclusive character. Our final target is to maintain that there is a room for fluent time in what is internal to points of view but external to the subjects adopting those points of view.