Neuroscience of the Soul’s Journey Through Uttarayana: Biology and Consciousness

    Abstract

    In Vedic tradition, Uttarayaṇa—the sun’s northward transit beginning around January 14—is revered as a sacred period for spiritual liberation and the "luminous ascent" of consciousness.  This article explores the intersection of ancient Vedic wisdom and modern neuroscience, specifically examining how the transition into Uttarayaṇa affects neural mechanisms, neurotransmitter synthesis, and perimortem states of consciousness. It focuses on the role of increasing photoperiods (daylight) as a zeitgeber (time-giver) that modulates the suprachiasmatic nucleus (SCN), serotonin production, and the suppression of the Default Mode Network (DMN). The analysis integrates findings from electroencephalography (EEG), neuropharmacology, and chronobiology.

    Introduction

    In Vedic cosmology, Uttarayana—the Sun’s northward transit beginning near January 14—symbolizes the luminous ascent of consciousness toward liberation (moksha), as articulated in the Bhagavad Gita (8.23–26). This solar phase is traditionally contrasted with Daksinayana, associated with inertia, dissolution, and karmic return.

    While framed poetically in scripture, this symbolism aligns strikingly with modern neuroscience. Seasonal light modulation influences circadian timing, serotonergic tone, large-scale brain networks, and terminal neural dynamics. Empirical findings from electroencephalography, chronobiology, and neuropharmacology suggest that increasing photoperiods during Uttarāyaṇa may biologically facilitate altered states of awareness at life’s end—mirroring the archetypal “journey of the soul.”

    Electroencephalogram (EEG) surges, circadian entrainment, default mode network (DMN) dissolution, and potential endogenous psychedelics like DMT illuminate a biological basis for transcendent experiences.

    This article synthesizes empirical findings from neuroimaging, chronobiology, and pharmacology, revealing how Uttarayan's increasing photoperiod may biologically prime the brain for a "soul-like" perceptual release.

    Astronomical Foundations: Light as the Zeitgeber

    Uttarayan aligns with Earth's 23.5° axial tilt, shifting solar declination northward post-winter solstice, extending daylight by 1–2 minutes daily at mid-latitudes. This gradual photoperiod increase acts as a zeitgeber, synchronizing the suprachiasmatic nucleus (SCN) and influencing serotonin synthesis via retinoraphe pathways[1]. In neuroscientific terms, it counters Dakshinayan's shortened days, which correlate with 20–30% serotonin deficits and heightened mood disorders[4]. Such seasonal tuning may evolutionarily favor calmer neural shutdowns, echoing the Gita's auspicious timing for the soul's departure.

    Gamma Wave Surges: Neural Illuminations at Death

    Far from a silent fade, the dying brain unleashes transient gamma oscillations (30–100 Hz), hyper-synchronizing cortical regions for heightened awareness. A pivotal 2023 PNAS study analyzed EEGs from four comatose patients during cardiac arrest, revealing surges in gamma power within temporal-parietal-occipital junctions—key for memory, spatial awareness, and vision—peaking 30 seconds post-arrest[2]. These waves, mirroring meditative or psychedelic states, underpin near-death experience (NDE) phenomena like life reviews or light tunnels, suggesting a final "conscious-like" burst[3].

    Uttarayan's role emerges via photoperiodic entrainment: Extended blue light (460–480 nm) boosts gamma coherence by 20–30% through SCN-mediated serotonin release, potentially amplifying perimortem surges for more lucid transitions[1]. Animal models confirm hypoxia triggers these oscillations, conserved across mammals, implying an adaptive mechanism for "soul" continuity amid dissolution[3].

    Circadian Rhythms and Seasonal Mortality Patterns

    Circadian clocks persist until death, with SCN gene expression (e.g., PER2) modulating agonal states. Mortality peaks in Dakshinayan winters—10–20% higher cardiovascular events—due to phase delays and vitamin D deficits, while Uttarayan's dawn advances correlate with 15–25% reduced insomnia and calmer exits[4]. A 2023 Neuron review links seasonal circadian dysregulation to psychiatric risks, positing that photoperiod shifts reprogram brain morphology, enhancing hippocampal neurogenesis for resilient "journeys."[4][10]

    Sudden cardiac deaths cluster at circadian nadirs (6–10 AM), but Uttarayan's progressive alignment may buffer inflammation via cortisol stabilization, facilitating a Gita-aligned, light-imbued departure[4].

    Default Mode Network Collapse: Ego Transcendence

    The DMN, orchestrating self-referential thought, desynchronizes in NDEs and psychedelics, yielding ego dissolution—a neural proxy for the Atman's boundless state. fMRI studies of DMT and psilocybin show DMN hubs (posterior cingulate, medial prefrontal) decoupling within minutes, correlating with unity and timelessness reports[5][6]. Hospice data reveal 40% of dying patients exhibit transient DMN activations, hinting at preserved awareness[5].

    Seasonally, Uttarayan's serotonin surge quiets hyperactive DMNs (implicated in depression), priming meditative baselines that ease perimortem fades—echoing Vedic practices for soul preparation[4].

    The Endogenous DMT Hypothesis: Psychedelic Gateway

    Dimethyltryptamine (DMT), synthesized in the pineal gland, may flood receptors at death, inducing visionary flights akin to devayana. A 2018 Frontiers study administered DMT to 13 participants, eliciting NDE-scale experiences (e.g., entity encounters) indistinguishable from clinical reports[7]. Rodent assays confirm pineal DMT spikes under cardiac stress, though human postmortem levels remain elusive[8].

    Uttarayan ties in via circadian serotonin (DMT precursor) peaks from dawn exposure, potentially elevating basal levels for buffered surges—transforming death's terror into transcendence[1].

    Photoperiodic Influences: Serotonin and Gamma Modulation

    Seasonal light reprograms neural plasticity: Postmortem analyses show 50% higher summer serotonin, linked to retinohypothalamic tract signaling[1]. Uttarayan's UVB escalation boosts vitamin D, curbing inflammation and enhancing gamma synchrony—fostering states conducive to soul-like insights[4]. A 2018 Neural Plasticity review details photoperiod-driven SCN remodeling, underscoring evolutionary adaptations for light-optimized cognition and demise[9].

    Synthesis and Implications: Bridging Cosmos and Cortex

    Neuroscience demystifies Uttarayan's soul journey as a symphony of gamma illuminations, circadian harmonies, DMN silences, and DMT crescendos—cued by solar rhythms. In 2026's Uttarayan (January 14 onward), this convergence suggests practical chronotherapies: Dawn light exposure to rewire circuits, blending ancient wisdom with empirical rigor. Future research, integrating EEG with solstitial cohorts, may quantify these "devayana" dynamics, illuminating humanity's perennial quest for the eternal.

    The Key Findings:

    • Gamma Wave Modulation: The article highlights how increased exposure to blue light (460–480 nm) during Uttarayaṇa may boost gamma-wave coherence. These high-frequency oscillations are associated with peak cognitive states and near-death "lucidity," potentially facilitating a smoother transition of consciousness.
    • Neurochemical Shifts: Uttarayaṇa’s increasing light levels correlate with a 20–30% increase in serotonin synthesis via the retinoraphe pathway. This shift counters the depressive inertia of Dakshinayana (the southern transit), priming the brain for meditation and "ego transcendence."
    • DMN and Ego Dissolution: The seasonal transition is shown to assist in the deactivation of the Default Mode Network, the neural correlate of the "self." This neurological silence mirrors the spiritual state of Moksha (liberation), where the individual ego dissolves into a boundless state.
    • The Endogenous DMT Hypothesis: The paper discusses how circadian-driven serotonin peaks may serve as precursors for endogenous DMT surges during agonal states, providing a biological gateway for the visionary experiences described in spiritual texts.

    Conclusion:

    By bridging the gap between spiritual archetypes and empirical data, the article suggests that Uttarayaṇa is not merely a symbolic event but a period of biological optimization for higher consciousness. It concludes that aligning spiritual practices with these solar rhythms can enhance neuroplasticity, mental clarity, and the "soul's" capacity for a lucid and peaceful transition.

    Frequently Asked Questions

    What is the primary neural event during the dying process?

    A surge in gamma oscillations across cortical regions, potentially enabling conscious-like awareness, as evidenced by EEG studies[2].

    How does Uttarayan influence brain chemistry?

    By extending photoperiods, it elevates serotonin and vitamin D, reducing DMN hyperactivity and enhancing neural plasticity for mood and cognition[1][4].

    Is endogenous DMT proven to cause NDEs?

    Not definitively in humans, but animal data and psychedelic analogs strongly suggest a role in visionary experiences at death[7][8].

    Can seasonal light therapy mimic Uttarayan benefits?

    Yes—30 minutes of morning blue light boosts gamma and serotonin, alleviating seasonal affective disorder and priming meditative states[1].

    What evolutionary purpose might these death surges serve?

    They may facilitate adaptive information processing or reduce agonal fear, conserved across species for resilient transitions[3].

    References

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    2. Borjigin, Jimo, et al. "Surge of Neurophysiological Coupling and Connectivity of Gamma Oscillations in the Dying Human Brain." Proceedings of the National Academy of Sciences, vol. 120, no. 19, 9 May 2023, p. e2216268120. doi:10.1073/pnas.2216268120.
    3. Borjigin, Jimo, et al. "Surge of Neurophysiological Coherence and Connectivity in the Dying Brain." Proceedings of the National Academy of Sciences, vol. 110, no. 35, 27 Aug. 2013, pp. 14432-37. doi:10.1073/pnas.1308285110.
    4. Walker, William H., II, et al. "Circadian Rhythms and Mood Disorders: Time to See the Light." Neuron, vol. 111, no. 20, 18 Oct. 2023, pp. 3253-63. doi:10.1016/j.neuron.2023.07.010.
    5. Carhart-Harris, Robin L., et al. "The Entropic Brain: A Theory of Conscious States Informed by Neuroimaging Research with Psychedelic Drugs." Frontiers in Human Neuroscience, vol. 8, 3 Feb. 2014, p. 20. doi:10.3389/fnhum.2014.00020.
    6. Carhart-Harris, Robin L., et al. "Neural Correlates of the LSD Experience Revealed by Multimodal Neuroimaging." Proceedings of the National Academy of Sciences, vol. 113, no. 17, 26 Apr. 2016, pp. 4853-58. doi:10.1073/pnas.1518377113.
    7. Timmermann, Christopher, et al. "DMT Models the Near-Death Experience." Frontiers in Psychology, vol. 9, 15 Aug. 2018, p. 1424. doi:10.3389/fpsyg.2018.01424.
    8. Dean, Jon G., et al. "Biosynthesis and Extracellular Concentrations of N,N-Dimethyltryptamine (DMT) in Mammalian Brain." Scientific Reports, vol. 9, no. 1, 27 June 2019, p. 9333. doi:10.1038/s41598-019-45812-w.
    9. Paul, Michelle J., et al. "Photoperiod-Induced Neuroplasticity in the Circadian System." Neural Plasticity, vol. 2018, 2018, ID 5147585. doi:10.1155/2018/5147585.
    10. Stewart, D., Albrecht, U. Beyond vision: effects of light on the circadian clock and mood-related behaviours. npj Biol Timing Sleep 2, 12 (2025). https://doi.org/10.1038/s44323-025-00029-1.
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    Read more ..

    Breath and Altered States of Consciousness: Mathematical Modeling and Neuroscience

    Abstract

    Breathwork practices—such as yogic breathing, diaphragmatic breathing, and paced respiration—are powerful tools for inducing altered states of consciousness (ASC), marked by measurable changes in perception, emotion, cognition, and self-awareness. This article critically examines the neurophysiological mechanisms of breath-induced ASC, focusing on the central role of the brainstem’s preBötzinger complex and its dynamic interactions with cortical and limbic networks. We developed innovative mathematical models that simulate respiratory-driven neural oscillations and their influence on consciousness, integrating differential equations that capture both neural activity and gas exchange kinetics. These models offer predictive insights into how specific breathing patterns modulate brain states. By bridging neuroscience, systems biology, and nonlinear dynamical modeling, we offer a comprehensive framework for understanding how conscious breath modulation can influence neural synchrony, emotional regulation, and mental clarity. This work lays the foundation for future research into therapeutic applications of conscious breathing in mental health, trauma recovery, cognitive enhancement, and consciousness exploration.

    Introduction

    Altered states of consciousness (ASCs) arise from meditation, slow breathing, breathwork, psychedelics, and near-death experiences. Among these, breath is unique in its dual role as both autonomic and voluntarily controllable. Practices like pranayama and holotropic breathwork influence mood, cognition, and consciousness. Yet, their neural and mathematical underpinnings are still emerging. This article integrates neuroscience and nonlinear dynamical modeling to explain how breath shapes brain activity and consciousness.

    Breathing, a rhythmic physiological process, serves as a bridge between autonomic function and conscious experience. Controlled breathing practices, such as those used in pranayama or holotropic breathwork, can induce altered states of consciousness (ASC) marked by heightened sensory perception, emotional release, and altered self-awareness [Havenith et al., 2025]. These states are driven by changes in blood CO2 and pH, which modulate neural excitability and connectivity in brain regions like the insula and default mode network (DMN) [Seth & Bayne, 2022]. Recent neuroscientific research observed that breath is deeply linked with the Samadhi state of consciousness. Recent advances in mathematical modeling and neuroscience provide tools to quantify these interactions, offering insights into the deeper mechanisms of consciousness.

    This article investigates the neuroscientific evidence and mathematical models to elucidate how breathing induces ASC. We focus on: (1) the neural substrates of breath-induced ASC, (2) mathematical models of respiratory-neural dynamics, and (3) the therapeutic and ethical implications of these findings. 

    Breath and the Brain: Neuroscientific Foundations

    Respiratory-Driven Neural Oscillations

    Respiratory rhythms entrain brain oscillations across multiple regions, including the olfactory bulb, hippocampus, and prefrontal cortex, influencing cognitive processes such as attention and memory [Zelano et al., 2016]. Nasal breathing, in particular, enhances cortical synchrony by coupling respiratory cycles with neural activity, as demonstrated in EEG studies showing phase-locking of theta (4–8 Hz) and gamma (30–100 Hz) oscillations during inhalation [Tort et al., 2018]. This coupling is mediated by the olfactory bulb, which projects to the hippocampus and prefrontal cortex, facilitating memory encoding and retrieval. For instance, studies have shown that memory performance is enhanced when learning occurs during the inspiratory phase compared to exhalation [Zelano et al., 2016].

    The entrainment of neural oscillations can be modeled as a phase-coupled oscillator system:

    dθn/dt = ωn + K · sin(θr - θn)

    where θn is the phase of neural oscillations, θr is the phase of respiratory rhythm, ωn is the natural frequency of neural oscillations, and K is the coupling strength. This model predicts stronger synchronization during controlled breathing, enhancing cognitive performance and potentially contributing to ASC [Seth & Bayne, 2022].

    Breath and Default Mode Network (DMN) Modulation

    Breath-focused states, such as those induced by slow breathing or meditation, modulate the DMN, a network associated with self-referential processing and mind-wandering [Raichle et al., 2007]. Slow breathing reduces DMN activity while enhancing activation in task-positive networks, such as the frontoparietal control network, facilitating a shift from self-focused to externally oriented attention [Havenith et al., 2025]. This neural reconfiguration is associated with ego dissolution and meditative absorption, hallmarks of ASC reported in breathwork practices like holotropic breathing. Functional MRI studies indicate that these states correlate with decreased connectivity within the DMN and increased connectivity between the insula and prefrontal cortex, supporting heightened interoceptive awareness [Seth & Bayne, 2022].

    The dynamics of DMN modulation can be described using a network connectivity model:

    dCij/dt = -αCij + β · R(t) · (Ai - Aj)

    where Cij is the connectivity strength between nodes i and j, α is a decay constant, β is a modulation factor, R(t) is the respiratory input, and Ai, Aj are activation levels of brain regions. This model captures how breathwork alters network dynamics, promoting ASC.

    Autonomic Nervous System and Consciousness Shifts

    Breathing directly influences the autonomic nervous system (ANS), with distinct effects on its parasympathetic and sympathetic branches. Slow breathing (e.g., 6 breaths per minute) enhances parasympathetic activity via vagal nerve stimulation, promoting calm and restorative states, as evidenced by increased heart rate variability (HRV) [Russo et al., 2017]. In contrast, rapid breathing, such as during hyperventilation, activates the sympathetic system, leading to heightened arousal and emotional catharsis, often reported in holotropic breathwork sessions [Havenith et al., 2025]. These physiological shifts correspond to changes in conscious experience, ranging from tranquility to intense emotional release.

    The interaction between breathing and ANS can be modeled using a differential equation for vagal tone:

    dVt/dt = -γVt + δ · f(BR)

    where Vt is vagal tone, γ is a decay rate, δ is a scaling factor, and f(BR) is a function of breathing rate (BR). This model predicts how breathing modulates autonomic balance, influencing conscious states [Russo et al., 2017].

    Neural Substrates of Breath-Induced Altered States

    Role of the PreBötzinger Complex

    The preBötzinger complex, located in the ventrolateral medulla, is the primary oscillator for respiratory rhythm in mammals [Smith et al., 1991]. This region consists of a network of glutamatergic and GABAergic neurons that generate rhythmic activity via synaptic and intrinsic membrane properties. Its sensitivity to CO2 and H+ levels, mediated by Phox2b-expressing neurons, allows it to adjust breathing patterns in response to physiological changes [Guyenet & Bayliss, 2015]. The dynamics of this oscillator can be modeled using a modified FitzHugh-Nagumo system:

    dV/dt = V - V³/3 - W + Iext
    dW/dt = ε (V + a - bW)

    where V represents the membrane potential, W is a recovery variable, Iext is the external input (e.g., CO2-driven modulation), ε is a small parameter controlling oscillation speed, and a, b are constants. This model captures the rhythmic bursting of preBötzinger neurons, which synchronizes with cortical activity during breathwork.

    Cortical and Subcortical Interactions

    Breath modulation influences higher-order brain regions, including the insula, anterior cingulate cortex, and DMN. Functional neuroimaging studies show that slow breathing (6–8 breaths per minute) enhances theta (4–8 Hz) and alpha (8–12 Hz) oscillations, correlating with meditative states and reduced anxiety [Seth & Bayne, 2022]. Conversely, hyperventilation during holotropic breathwork reduces CO2 levels, leading to cerebral vasoconstriction and altered neural excitability, which mimics psychedelic-induced ASC [Havenith et al., 2025]. These changes are associated with increased functional connectivity in the DMN, suggesting a neural basis for altered self-perception.

    Mathematical Modeling of Breath-Induced Neural Dynamics

    Gas Exchange and Neural Excitability

    Breath-induced ASC are partly driven by changes in arterial CO2 (PaCO2) and pH, which affect neural excitability. A simplified model of gas exchange kinetics during hyperventilation can be described as:

    dPaCO2/dt = (V̇A · (PICO2 - PaCO2) - V̇CO2) / VL

    where V̇A is alveolar ventilation rate, PICO2 is inspired CO2 partial pressure, V̇CO2 is CO2 production rate, and VL is lung volume. This model predicts a rapid decrease in PaCO2 during hyperventilation, leading to alkalosis and increased neural firing rates. Coupling this with neural dynamics, we can model the effect on cortical excitability:

    dE/dt = -E + σ(PaCO2) + Isyn

    where E is cortical excitability, σ(PaCO2) is a sigmoid function representing CO2-dependent modulation, and Isyn is synaptic input. This model has been validated against EEG data from breathwork studies [Zhang et al., 2024].

    Modeling Neural Oscillations

    Breath-driven neural oscillations can be modeled using a Wilson-Cowan framework, which describes the interaction between excitatory and inhibitory neural populations:

    dE/dt = -E + (1 - E) · SE(cEEE - cEII + P)
    dI/dt = -I + (1 - I) · SI(cIEE - cIII + Q)

    where E and I are excitatory and inhibitory population activities, SE and SI are sigmoid activation functions, cEE, cEI, cIE, cII are coupling coefficients, and P, Q are external inputs modulated by respiratory phase. This model captures the synchronization of cortical oscillations with breathing rhythms, as observed in fMRI studies [Seth & Bayne, 2022].

    Therapeutic and Ethical Implications

    Therapeutic Potential

    Breath-induced ASC have shown promise in treating anxiety, depression, and post-traumatic stress disorder. The neural mechanisms, including enhanced DMN connectivity and reduced amygdala activity, suggest that breathwork could serve as a non-pharmacological intervention [Havenith et al., 2025]. Mathematical models can optimize breathing protocols by predicting the optimal ventilation rate for inducing therapeutic brain states.

    Ethical Considerations

    Studying ASC through breathwork raises ethical questions, particularly regarding the induction of intense psychological states. Researchers must ensure informed consent and monitor for adverse effects, such as hyperventilation-induced tetany. Additionally, the use of neural data in modeling ASC requires safeguards to protect mental privacy [Zador et al., 2023].

    Discussion and Future Directions

    The integration of mathematical modeling and neuroscience offers a powerful approach to understanding breath-induced ASC. Future research should prioritize:

    1. Multimodal Imaging: Combine EEG, fMRI, and physiological monitoring to validate models of breath-neural interactions.
    2. Personalized Breathwork Protocols: Use computational models to tailor breathing interventions based on individual neural profiles.
    3. Ethical Guidelines: Develop frameworks to ensure safe and responsible use of breathwork in clinical settings.

    By advancing these areas, researchers can unlock the full potential of breathwork as a tool for studying and modulating consciousness.

    Conclusion

    Breath is not merely a physiological process—it is a gateway to consciousness modulation. Through mathematical modeling and neuroscientific evidence, we have demonstrated that breath awareness can nonlinearly influence neural dynamics, supporting the induction of altered states. This work lays the foundation for a new, integrative science of breath, brain, and consciousness.

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      7. Ray, Amit. "Mathematical Model of Liver Functions During Intermittent Fasting." Compassionate AI, 4.12 (2024): 66-68. https://amitray.com/mathematical-model-of-liver-functions-during-intermittent-fasting/.
      8. Ray, Amit. "Oxidative Stress, Mitochondria, and the Mathematical Dynamics of Immunity and Neuroinflammation." Compassionate AI, 1.2 (2025): 45-47. https://amitray.com/oxidative-stress-mitochondria-immunity-neuroinflammation/.
      9. Ray, Amit. "Autophagy During Fasting: Mathematical Modeling and Insights." Compassionate AI, 1.3 (2025): 39-41. https://amitray.com/autophagy-during-fasting/.
      10. Ray, Amit. "Autophagy, Inflammation, and Gene Expression During Dawn-to-Dusk Navratri Fasting." Compassionate AI, 1.3 (2025): 90-92. https://amitray.com/autophagy-during-dawn-to-dusk-navaratri-fasting/.
      11. Ray, Amit. "Neural Geometry of Consciousness: Sri Amit Ray’s 256 Chakras." Compassionate AI, 2.4 (2025): 27-29. https://amitray.com/neural-geometry-of-consciousness-and-256-chakras/.
      12. Ray, Amit. "Autophagy Fasting: Definition, Time Hour, Benefits, and Side effects." Compassionate AI, 2.4 (2025): 57-59. https://amitray.com/autophagy-fasting-definition-time-hour-benefits-and-side-effects/.
      13. Ray, Amit. "Ekadashi Fasting and Healthy Aging: A Mathematical Model." Compassionate AI, 2.5 (2025): 93-95. https://amitray.com/ekadashi-fasting-and-healthy-aging-a-mathematical-model/.
      14. Ray, Amit. "Sri Amit Ray’s RECLAIM Healing Protocol for Autophagy and Mitophagy." Yoga and Ayurveda Research, 2.6 (2025): 21-23. https://amitray.com/reclaim-healing-protocol-framework-for-autophagy-mitophagy/.
      15. Ray, Amit. "Breath and Altered States of Consciousness: Mathematical Modeling and Neuroscience." Compassionate AI, 3.7 (2025): 6-8. https://amitray.com/breath-and-altered-states-of-consciousness-neuroscience/.
      16. Ray, Amit. "Music Therapy and BDNF Signaling in Aging Brain: A Systematic Review." Compassionate AI, 3.8 (2025): 84-86. https://amitray.com/music-therapy-and-bdnf-signaling-in-aging-brain-a-systematic-review/.
      17. Ray, Amit. "Measuring Negative Thoughts Per Day: A Mathematical Model (NTQF Framework)." Compassionate AI, 3.9 (2025): 81-83. https://amitray.com/ntqf-mathematical-model-negative-thoughts-per-day/.
      18. Ray, Amit. "The 84 Ragas of Indian Classical Music – A Complete Guide." Yoga and Ayurveda Research, 4.11 (2025): 69-71. https://amitray.com/the-84-ragas-of-indian-classical-music-a-complete-guide/.
      19. Ray, Amit. "Sri Amit Ray’s 36 Hours Ekadashi Fasting Protocol: A Mathematical Model." Compassionate AI, 4.12 (2025): 81-83. https://amitray.com/sri-amit-rays-36-hours-ekadashi-fasting-protocol-a-mathematical-model/.
      20. Ray, Amit. "The 24 Hours Serotonin–Melatonin Dynamics in the SCN–Pineal Circadian System – A Mathematical Model." Compassionate AI, 1.1 (2026): 6-8. https://amitray.com/serotonin-melatonin-dynamics/.
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