**1. Introduction**

Anxiety is associated with psychological states that consubstantially ignite an imbalance with the neuroimmune system. For example, cancer anxiety has been associated with a decrease in natural killer (NK) cells [1]. It is well established that care-givers of the terminally ill score higher than non-family members on the Hospital Anxiety and Depression Scale (HADS); but over time, this value decreases as the family member adapts to the worsening condition of their loved one [2]. These aspects of anxiety obtain neural correlates that are both endocrine stress hormone-linked and epigenetic in origin, with links to the immune system. Combined

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

with an environment of stress, immune responses can epigenetically alter the expression of genetic loci and potentially modify those genes directly. This association of stress with later anxiety manifestation may have deeper roots going back to in utero events affecting the neuroimmunoepigenome of the fetus.

The interplay of organisms is the macrocosm, but it also appropriately describes the human body and overall stress imposed by the microbiome, invading pathogens, autoimmunity, cancer, autophagy, and senescence. The development, differentiation, and the signal transduction cascade network, including neuronal action potentials and endocrine mediation, also compose an opposing three-dimensional trigonal plane where the central element is the homeostasis of the existing individual. Indeed, learning and the accumulation of memories and knowledge are all part of a massive internal interactome that can be understood relative to advantage, vectorial control, and constant failure. Anxiogenesis can arise from perturbations to this system and manifest at the physiological and neuropsychological level.

There is a natural-native system that encompasses all of the features describing this neuropsychiatric interactome and its axis is the immune system. Thus, the immune system has two roles in the human body. One is for defense plus offense, and the other, in conjunction with epigenetic mechanisms, generates the existing individual. This is a perpetuating neural network that can learn, via attention and ascent to stress, to function within the world. Such a biologically adaptive phenomenon is accomplished via homologous recombination of variable regions of both the immunoglobulin family and the T-cell receptor in concert with chromatin remodeling, the histone code, and both the acetylome and methylome of cohering DNA. If there is a link between the mind and the body, at least one component is physical. This connection might be the molecular and cellular adaptive immunological interactome that serves to generate neural tracts according to developmental, endocrine, and peripheral stimuli while maintaining repair processes in the central nervous system (CNS) by using the complex interactions between microglia and neurons. Neural networks are processes, becoming eventual in nature, as contrasted with a substance ontology. The pattern of events appears as energetic fields rather than particles of matter, much like chemical bonds. An event ontology that reaches across the neural network of genetic and environmental interaction is articulated and synthesized through epigenetic modifications of the classical immune system, thus creating a responsive plastic and elastic memory field capable of learning, ideation, imagination, and understanding through time. This diaeventome involves the central existing individual agentically interacting through the events obtained across the inherited genome, the changing environment, and the transcendental immunoepigenome through time.

metabolic response to the micro- and macro-environment through classical constitutivesurveillance and acquired-effector cellular and humoral defense stratagems using reversible covalent modification and hydrophobic interactions of nucleic acids, proteins, and lipids.

The Diaeventology of Anxiety Disorders http://dx.doi.org/10.5772/intechopen.82176 15

Thus, I will explore how diaeventology offers a general molecular system theory for a free will-driven/agency-based individual adaptation and a knowledge-acquiring physiologicorational mechanism that better explains the core event ontology of human existence including

During early stages of embryo implantation, there is a suggested suppression of the immune response; yet, there are many immune systems at play. These include NK cells. NKs are innate immune cells that require no secondary or tertiary recombination and adaptation to kill target cells upon antigen presentation as with Major Histocompatibility Complex (MHC) class I-held antigens [3]. This allows NK cells to degranulate and release cytotoxic substances directly into targeted cells for destruction. There is a pull back, or switch, that may involve mesenchymal stem cells signaling through interferon that regulate and therefore license and

delicense the NK killing based on chemokine reception and a global on/off switch [3].

A recent report catalogs some of the descriptors of immune surveillance in the uterus. In this chapter, it is reported that macrophages, NK cells, and T cells are found in the human decidua [3]. Over 70% of the detectable immune cells are NKs and the rest are mostly macrophages with small percentages of dendritic cells. They also summarize from the literature that no B or plasma cells can be detected. However, the remainder of the immune cell population is of

health and well-being.

**Figure 1.** The diaeventome paradigm.

T-cell lineage.

**2. Diaeventological sources of GAD**

### **Figure 1** represents the current model.

This chapter will employ my new paradigm of diaeventology to introduce and instantiate the neural correlative endophenotype linked to the psychiatric condition general anxiety disorder (GAD).

Diaeventology (dialectical event ontology) is an adaptational, processive scientific accounting of the physiologico-rational human condition through cellular and molecular event ontology.

Its biological mechanism of action, linking pathopsychological states like GAD to biochemical pathways, incorporates the immuno-epigenomic induction of neural, endocrine, and

**Figure 1.** The diaeventome paradigm.

with an environment of stress, immune responses can epigenetically alter the expression of genetic loci and potentially modify those genes directly. This association of stress with later anxiety manifestation may have deeper roots going back to in utero events affecting the neu-

The interplay of organisms is the macrocosm, but it also appropriately describes the human body and overall stress imposed by the microbiome, invading pathogens, autoimmunity, cancer, autophagy, and senescence. The development, differentiation, and the signal transduction cascade network, including neuronal action potentials and endocrine mediation, also compose an opposing three-dimensional trigonal plane where the central element is the homeostasis of the existing individual. Indeed, learning and the accumulation of memories and knowledge are all part of a massive internal interactome that can be understood relative to advantage, vectorial control, and constant failure. Anxiogenesis can arise from perturba-

tions to this system and manifest at the physiological and neuropsychological level.

the changing environment, and the transcendental immunoepigenome through time.

This chapter will employ my new paradigm of diaeventology to introduce and instantiate the neural correlative endophenotype linked to the psychiatric condition general anxiety disorder

Diaeventology (dialectical event ontology) is an adaptational, processive scientific accounting of the physiologico-rational human condition through cellular and molecular event ontology. Its biological mechanism of action, linking pathopsychological states like GAD to biochemical pathways, incorporates the immuno-epigenomic induction of neural, endocrine, and

There is a natural-native system that encompasses all of the features describing this neuropsychiatric interactome and its axis is the immune system. Thus, the immune system has two roles in the human body. One is for defense plus offense, and the other, in conjunction with epigenetic mechanisms, generates the existing individual. This is a perpetuating neural network that can learn, via attention and ascent to stress, to function within the world. Such a biologically adaptive phenomenon is accomplished via homologous recombination of variable regions of both the immunoglobulin family and the T-cell receptor in concert with chromatin remodeling, the histone code, and both the acetylome and methylome of cohering DNA. If there is a link between the mind and the body, at least one component is physical. This connection might be the molecular and cellular adaptive immunological interactome that serves to generate neural tracts according to developmental, endocrine, and peripheral stimuli while maintaining repair processes in the central nervous system (CNS) by using the complex interactions between microglia and neurons. Neural networks are processes, becoming eventual in nature, as contrasted with a substance ontology. The pattern of events appears as energetic fields rather than particles of matter, much like chemical bonds. An event ontology that reaches across the neural network of genetic and environmental interaction is articulated and synthesized through epigenetic modifications of the classical immune system, thus creating a responsive plastic and elastic memory field capable of learning, ideation, imagination, and understanding through time. This diaeventome involves the central existing individual agentically interacting through the events obtained across the inherited genome,

roimmunoepigenome of the fetus.

14 Anxiety Disorders - From Childhood to Adulthood

**Figure 1** represents the current model.

(GAD).

metabolic response to the micro- and macro-environment through classical constitutivesurveillance and acquired-effector cellular and humoral defense stratagems using reversible covalent modification and hydrophobic interactions of nucleic acids, proteins, and lipids.

Thus, I will explore how diaeventology offers a general molecular system theory for a free will-driven/agency-based individual adaptation and a knowledge-acquiring physiologicorational mechanism that better explains the core event ontology of human existence including health and well-being.
