Years
2026
Categories
Authors
ARTICLES
Review Article
Disinhibition: A Conceptual Hypothesis to Explain Near-Death Experiences And Out-of-Body Experiences
Turkish Title : Disinhibition: A Conceptual Hypothesis to Explain Near-Death Experiences And Out-of-Body Experiences
Lugten Peter
JNBS, 2026, 13(2), p:75-85
Living beings bring more order to the world, and are required by the second law of thermodynamics, to simultaneously produce more disorder through metabolic heat dissipation. Consciousness in living beings produces even more order, enhancing survival and reproduction, and incurs an entropy debt that must be paid separately, and non-metabolically, through heat dissipation produced by Landauer’s principle: the erasure of information within the "explanatory gap" of the hard problem. Consciousness is assumed to depend on the properties of tryptophan in microtubules and their ability to dissipate heat through superradiation as required by Landauer. After the post-mortem decomposition of microtubules, consciousness will have no mechanism for the necessary heat discharge, which would violate Landauer’s principle and thus the second law. Any actual such survival would imply life-before-death to be solipsism. The aim is to distinguish near-death experiences and out-of-body experiences from life-after-death in biophysical terms, and to explain how they might arise as a result of natural forces. It is hypothesized that near-death and out-of-body experiences, and their vivid nature, arise from the disinhibition of microtubular consciousness after electroencephalographic brain activity has stopped, but while microtubular Tryptophan continues to be activated by ultraviolet photons. These are hypothesized to be transmitted to the brain primarily via light falling on the retina or skin, carried to the brain through mitochondria and microtubules acting as optical waveguides. Additionally, bioluminescent ultra-weak photon emissions accompany membrane depolarization at the moment of death. It is hypothesized that the relativistic transactional interpretation of quantum mechanics could explain the entanglement of this photonic microtubular input, as potentialities, with environmental photons in order to account for rare, veridical near-death extraocular perceptions. Veridical Auditory near-death and out-of-body experiences require a coordinated stimulation of Heschl’s gyrus by ambient sound, which might be accomplished by adiabatic mechanical propulsion of axonal solitons along the Auditory nerve, or possibly transcranial perception of low frequency sound waves.Ultimately, the approach of death can be accompanied by a pseudo-solipsism of "added time" that could seem like an eternity for the deceased person even as microtubular stimulation decreases.
Living beings bring more order to the world, and are required by the second law of thermodynamics, to simultaneously produce more disorder through metabolic heat dissipation. Consciousness in living beings produces even more order, enhancing survival and reproduction, and incurs an entropy debt that must be paid separately, and non-metabolically, through heat dissipation produced by Landauer’s principle: the erasure of information within the "explanatory gap" of the hard problem. Consciousness is assumed to depend on the properties of tryptophan in microtubules and their ability to dissipate heat through superradiation as required by Landauer. After the post-mortem decomposition of microtubules, consciousness will have no mechanism for the necessary heat discharge, which would violate Landauer’s principle and thus the second law. Any actual such survival would imply life-before-death to be solipsism. The aim is to distinguish near-death experiences and out-of-body experiences from life-after-death in biophysical terms, and to explain how they might arise as a result of natural forces. It is hypothesized that near-death and out-of-body experiences, and their vivid nature, arise from the disinhibition of microtubular consciousness after electroencephalographic brain activity has stopped, but while microtubular Tryptophan continues to be activated by ultraviolet photons. These are hypothesized to be transmitted to the brain primarily via light falling on the retina or skin, carried to the brain through mitochondria and microtubules acting as optical waveguides. Additionally, bioluminescent ultra-weak photon emissions accompany membrane depolarization at the moment of death. It is hypothesized that the relativistic transactional interpretation of quantum mechanics could explain the entanglement of this photonic microtubular input, as potentialities, with environmental photons in order to account for rare, veridical near-death extraocular perceptions. Veridical Auditory near-death and out-of-body experiences require a coordinated stimulation of Heschl’s gyrus by ambient sound, which might be accomplished by adiabatic mechanical propulsion of axonal solitons along the Auditory nerve, or possibly transcranial perception of low frequency sound waves.Ultimately, the approach of death can be accompanied by a pseudo-solipsism of "added time" that could seem like an eternity for the deceased person even as microtubular stimulation decreases.
Review Article
Neurotoxic Effects of Electronic Cigarette Exposure on the Central Nervous System: A Scoping Review
Turkish Title : Neurotoxic Effects of Electronic Cigarette Exposure on the Central Nervous System: A Scoping Review
Emre Taner Özcan
JNBS, 2026, 13(2), p:86-103
Electronic cigarettes (e-cigarettes) have achieved global adoption, with an estimated 82 million users worldwide and disproportionate uptake among adolescents. Despite marketing as a safer tobacco alternative, e-cigarette aerosols contain neurotoxic constituents including nicotine, flavoring agents, carbonyl compounds, and heavy metals. This review maps empirical evidence on CNS effects of e-cigarette exposure across biological model types. A systematic scoping review was conducted per the Arksey and O'Malley framework and reported per PRISMA-ScR guidelines. PubMed and Scopus were searched in January 2026 for studies from 2015 to 2026 examining quantifiable CNS outcomes following e-cigarette exposure in human, animal, or in vitro models. Data were extracted across eight domains and synthesized narratively. Seventy-four studies met inclusion criteria: 49 animal in vivo (66.2%), 17 human (23.0%), and 8 in vitro (10.8%), spanning 14 countries. Seven CNS outcome domains were identified: neuroinflammation and oxidative stress, blood-brain barrier (BBB) integrity, cognitive and behavioral outcomes, neuroimaging and pharmacokinetics, neurotransmitter systems and electrophysiology, developmental neurotoxicology, and other outcomes. Neuroinflammation and BBB disruption showed high directional consistency. Cognitive impairment, hippocampal volume reductions, and reward circuit reorganization were consistently observed. Developmental studies identified epigenomic reprogramming and disrupted GABAergic interneuron migration. Non-nicotine constituents were independently implicated in CNS toxicity. E-cigarette exposure is associated with a consistent and biologically plausible pattern of CNS harm. The developing brain represents a priority risk population. Current evidence does not support the neurological safety of e-cigarettes; regulatory frameworks should mandate CNS-specific toxicity assessment for electronic nicotine delivery systems.
Electronic cigarettes (e-cigarettes) have achieved global adoption, with an estimated 82 million users worldwide and disproportionate uptake among adolescents. Despite marketing as a safer tobacco alternative, e-cigarette aerosols contain neurotoxic constituents including nicotine, flavoring agents, carbonyl compounds, and heavy metals. This review maps empirical evidence on CNS effects of e-cigarette exposure across biological model types. A systematic scoping review was conducted per the Arksey and O'Malley framework and reported per PRISMA-ScR guidelines. PubMed and Scopus were searched in January 2026 for studies from 2015 to 2026 examining quantifiable CNS outcomes following e-cigarette exposure in human, animal, or in vitro models. Data were extracted across eight domains and synthesized narratively. Seventy-four studies met inclusion criteria: 49 animal in vivo (66.2%), 17 human (23.0%), and 8 in vitro (10.8%), spanning 14 countries. Seven CNS outcome domains were identified: neuroinflammation and oxidative stress, blood-brain barrier (BBB) integrity, cognitive and behavioral outcomes, neuroimaging and pharmacokinetics, neurotransmitter systems and electrophysiology, developmental neurotoxicology, and other outcomes. Neuroinflammation and BBB disruption showed high directional consistency. Cognitive impairment, hippocampal volume reductions, and reward circuit reorganization were consistently observed. Developmental studies identified epigenomic reprogramming and disrupted GABAergic interneuron migration. Non-nicotine constituents were independently implicated in CNS toxicity. E-cigarette exposure is associated with a consistent and biologically plausible pattern of CNS harm. The developing brain represents a priority risk population. Current evidence does not support the neurological safety of e-cigarettes; regulatory frameworks should mandate CNS-specific toxicity assessment for electronic nicotine delivery systems.
Review Article
Investigation of the Effects of the Gut-Brain Axis on Brain and Mental Health
Turkish Title : Investigation of the Effects of the Gut-Brain Axis on Brain and Mental Health
Balcı Feride Nihal
JNBS, 2026, 13(1), p:30-39
There is a bidirectional and continuous relationship and communication between the brain and the gut. The gut-brain axis communicates not only through the microbiota but also via the autonomic nervous system. Microorganisms in the gut microbiota are known to contribute to the production of certain neurotransmitters that play roles in brain function, which may, in turn, influence mental health. Through this interaction, the gut microbiota and gastrointestinal system components play significant roles in human health. A healthy functioning of the gut-brain axis is essential for supporting the immune system, regulating mood, and maintaining cognitive and immune health. Recent studies highlight a connection and causality between the gut-brain-microbiota axis and neurological disorders such as Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, and autism spectrum disorder, as well as psychiatric disorders like depression, anxiety, schizophrenia, and bipolar disorder. This paper reviews the impact of the gut-brain-microbiota axis on brain and mental health, emotion-thought-behavior systems, and its effects on neurological and psychiatric disorders.
There is a bidirectional and continuous relationship and communication between the brain and the gut. The gut-brain axis communicates not only through the microbiota but also via the autonomic nervous system. Microorganisms in the gut microbiota are known to contribute to the production of certain neurotransmitters that play roles in brain function, which may, in turn, influence mental health. Through this interaction, the gut microbiota and gastrointestinal system components play significant roles in human health. A healthy functioning of the gut-brain axis is essential for supporting the immune system, regulating mood, and maintaining cognitive and immune health. Recent studies highlight a connection and causality between the gut-brain-microbiota axis and neurological disorders such as Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, and autism spectrum disorder, as well as psychiatric disorders like depression, anxiety, schizophrenia, and bipolar disorder. This paper reviews the impact of the gut-brain-microbiota axis on brain and mental health, emotion-thought-behavior systems, and its effects on neurological and psychiatric disorders.
| ISSN (Print) | 2149-1909 |
| ISSN (Online) | 2148-4325 |
2020 Ağustos ayından itibaren yalnızca İngilizce yayın kabul edilmektedir.

