Can A Quantum Field Theory Ontology Help Resolve the Problem of Consciousness?

The hard problem of consciousness arises in most incarnations of present day physicalism. Why should certain physical processes necessarily be accompanied by experience? One possible response is that physicalism itself should be modified in order to accommodate experience: But, modified how? In the present work, we investigate whether an ontology derived from quantum field theory can help resolve the hard problem. We begin with the assumption that experience cannot exist without being accompanied by a subject of experience (SoE). While people well versed in Indian philosophy will not find that statement problematic, it is still controversial in the analytic tradition. Luckily for us, Strawson has elaborately defended the notion of a thin subject—an SoE which exhibits a phenomenal unity with different types of content (sensations, thoughts etc.) occurring during its temporal existence. Next, following Stoljar, we invoke our ignorance of the true physical as the reason for the explanatory gap between present day physical processes (events, properties) and experience. We are therefore permitted to conceive of thin subjects as related to the physical via a new, yet to be elaborated relation. While this is difficult to conceive under most varieties of classical physics, we argue that this may not be the case under certain quantum field theory ontologies. We suggest that the relation binding an SoE to the physical is akin to the relation between a particle and (quantum) field. In quantum field theory, a particle is conceived as a coherent excitation of a field. Under the right set of circumstances, a particle coalesces out of a field and dissipates. We suggest that an SoE can be conceived as akin to a particle—a SelfOn—which coalesces out of physical fields, persists for a brief period of time and then dissipates in a manner similar to the phenomenology of a thin subject. Experiences are physical properties of selfons with the constraint (specified by a similarity metric) that selfons belonging to the same natural kind will have similar experiences. While it is odd at first glance to conceive of subjects of experience as akin to particles, the spatial and temporal unity exhibited by particles as opposed to fields and the expectation that selfons are new kinds of particles, paves the way for cementing this notion. Next, we detail the various no-go theorems in most versions of quantum field theory and discuss their impact on the existence of selfons. Finally, we argue that the time is ripe for a rejuvenated Indian philosophy to begin tackling the three-way relationship between SoEs (which may become equivalent to jivas in certain Indian frameworks), phenomenal content and the physical world. With analytic philosophy still struggling to come to terms with the complex worlds of quantum field theory and with the relative inexperience of the western world in arguing the jiva-world relation, there is a clear and present opportunity for Indian philosophy to make a worldcentric contribution to the hard problem of experience

Pathogenesis of adolescent idiopathic scoliosis in girls - a double neuro-osseous theory involving disharmony between two nervous systems, somatic and autonomic expressed in the spine and trunk: possible dependency on sympathetic nervous system and hormones with implications for medical therapy

Anthropometric data from three groups of adolescent girls - preoperative adolescent idiopathic scoliosis (AIS), screened for scoliosis and normals were analysed by comparing skeletal data between higher and lower body mass index subsets. Unexpected findings for each of skeletal maturation, asymmetries and overgrowth are not explained by prevailing theories of AIS pathogenesis. A speculative pathogenetic theory for girls is formulated after surveying evidence including: (1) the thoracospinal concept for right thoracic AIS in girls; (2) the new neuroskeletal biology relating the sympathetic nervous system to bone formation/resorption and bone growth; (3) white adipose tissue storing triglycerides and the adiposity hormone leptin which functions as satiety hormone and sentinel of energy balance to the hypothalamus for long-term adiposity; and (4) central leptin resistance in obesity and possibly in healthy females. The new theory states that AIS in girls results from developmental disharmony expressed in spine and trunk between autonomic and somatic nervous systems. The autonomic component of this double neuro-osseous theory for AIS pathogenesis in girls involves selectively increased sensitivity of the hypothalamus to circulating leptin (genetically-determined up-regulation possibly involving inhibitory or sensitizing intracellular molecules, such as SOC3, PTP-1B and SH2B1 respectively), with asymmetry as an adverse response (hormesis); this asymmetry is routed bilaterally via the sympathetic nervous system to the growing axial skeleton where it may initiate the scoliosis deformity (leptin-hypothalamic-sympathetic nervous system concept = LHS concept). In some younger preoperative AIS girls, the hypothalamic up-regulation to circulating leptin also involves the somatotropic (growth hormone/IGF) axis which exaggerates the sympathetically-induced asymmetric skeletal effects and contributes to curve progression, a concept with therapeutic implications. In the somatic nervous system, dysfunction of a postural mechanism involving the CNS body schema fails to control, or may induce, the spinal deformity of AIS in girls (escalator concept). Biomechanical factors affecting ribs and/or vertebrae and spinal cord during growth may localize AIS to the thoracic spine and contribute to sagittal spinal shape alterations. The developmental disharmony in spine and trunk is compounded by any osteopenia, biomechanical spinal growth modulation, disc degeneration and platelet calmodulin dysfunction. Methods for testing the theory are outlined. Implications are discussed for neuroendocrine dysfunctions, osteopontin, sympathoactivation, medical therapy, Rett and Prader-Willi syndromes, infantile idiopathic scoliosis, and human evolution. AIS pathogenesis in girls is predicated on two putative normal mechanisms involved in trunk growth, each acquired in evolution and unique to humans

Interleukin 6 deficiency modulates the hypothalamic expression of energy balance regulating peptides during pregnancy in mice.

Pregnancy is associated with hyperphagia, increased adiposity and multiple neuroendocrine adaptations. Maternal adipose tissue secretes rising amounts of interleukin 6 (IL6), which acts peripherally modulating metabolic function and centrally increasing energy expenditure and reducing body fat. To explore the role of IL6 in the central mechanisms governing dam's energy homeostasis, early, mid and late pregnant (gestational days 7, 13 and 18) wild-type (WT) and Il6 knockout mice (Il6-KO) were compared with virgin controls at diestrus. Food intake, body weight and composition as well as indirect calorimetry measurements were performed in vivo. Anabolic and orexigenic peptides: neuropeptide Y (Npy) and agouti-related peptide (Agrp); and catabolic and anorectic neuropeptides: proopiomelanocortin (Pomc), corticotrophin and thyrotropin-releasing hormone (Crh and Trh) mRNA levels were determined by in situ hybridization. Real time-PCR and western-blot were used for additional tissue gene expression and protein studies. Non-pregnant Il6-KO mice were leaner than WT mice due to a decrease in fat but not in lean body mass. Pregnant Il6-KO mice had higher fat accretion despite similar body weight gain than WT controls. A decreased fat utilization in absence of Il6 might explain this effect, as shown by increased respiratory exchange ratio (RER) in virgin Il6-KO mice. Il6 mRNA levels were markedly enhanced in adipose tissue but reduced in hypothalamus of mid and late pregnant WT mice. Trh expression was also stimulated at gestational day 13 and lack of Il6 blunted this effect. Conversely, in late pregnant mice lessened hypothalamic Il6 receptor alpha (Il6ra), Pomc and Crh mRNA were observed. Il6 deficiency during this stage up-regulated Npy and Agrp expression, while restoring Pomc mRNA levels to virgin values. Together these results demonstrate that IL6/IL6Ra system modulates Npy/Agrp, Pomc and Trh expression during mouse pregnancy, supporting a role of IL6 in the central regulation of body fat in this physiological state