A cinematic journey from collapse to awakening
Tobias Sinclair’s collapse wasn’t just medical—it was a rupture in perception. From that moment, a theory emerged: our universe may behave like a subatomic particle, nested within something far greater.
This short film explores the birth of The New Science—a movement that challenges our view of scale, energy, and consciousness - and the architecture of reality.
What if healing one life could awaken a species? What if the universe… is watching us back?
“This isn’t a rejection of science—it’s a reframing.”
🧩 Summary of Tobias’s “New Science” Proposition
Tobias Sinclair presents a metaphysical reinterpretation of established physics, blending poetic analogy with speculative cosmology:
🔹 Key Ideas
🔬 Comparison to Current Theoretical Physics
✅ Points of Conceptual Overlap
Tobias’s Idea
1. Universe as a particle
2. Nested universes
3. Scale-dependent laws
4. Frequency of universe
Physics Parallel
1. Echoes multiverse and holographic principle concepts
2. Reminiscent of brane cosmology in string theory
3. Reflects the challenge of quantum gravity and unification
4. Loosely parallels cosmic microwave background and wave-particle duality
❌ Points of Departure from Scientific Consensus
🧠 What Physicists Are Actually Exploring
🧭 Verdict: Visionary but Unverified
Tobias’s “New Science” is a compelling philosophical and narrative device. It creatively reimagines physics through metaphor and recursive logic, offering a fresh lens on cosmic unity. However:
Still, it resonates with the spirit of inquiry that drives physics forward. Tobias isn’t trying to disprove science—he’s trying to reframe it.
The book
🧠 Tobias’s Leap: Nested Universes Within Electrons
Tobias proposes that:
This is not a literal reinterpretation of Einstein’s equation, but a symbolic one—suggesting that energy arises from relational motion between entities, not just intrinsic mass.
🔬 Mainstream Physics: What’s Actually Being Explored
Recent theoretical work does entertain ideas that echo Tobias’s metaphor, though not in the same form:
🔹 1. Multiverse and Brane Cosmology
🔹 2. Anthropic Reasoning and Nested Structures
🔹 3. Quantum Multiverse (Many Worlds Interpretation)
🔹 4. Holographic Principle
🧭 Verdict: Metaphor Meets Mystery
Tobias’s idea of nested universes within electrons is not part of mainstream physics—but it resonates with several speculative frameworks:
Concept
1. Nested universes
2. Scale inversion
3. Energy from interaction
4. Quantum–relativity bridge
Tobias’s View
1. Electrons contain entire universes
2. Universe behaves like a particle
3. E = mc² reinterpreted as relational
4. Scale determines governing laws
Physics Parallel
1. Brane cosmology, anthropic multiverse
2. Holographic principle, fractal cosmology
3. Not supported mathematically, but metaphorically rich
4. Still an open problem in physics
🧠 Tobias’s Core Proposal
Tobias suggests:
🔬 Feasibility Based on Current Physics
✅ Conceptual Parallels
❌ Scientific Challenges
🧪 Recent Speculations
🧭 Verdict: Metaphorically Rich, Physically Unproven
Tobias’s theory is not feasible in the strict scientific sense—but it’s philosophically provocative and conceptually resonant with speculative physics. It reframes known observations through a lens of recursive scale and relational motion, offering a poetic bridge between quantum and cosmic realms.
Rather than replacing physics, Tobias’s New Science invites us to reimagine its implications—a creative act that has historically led to breakthroughs.
🧬 Tobias’s New Science: A Fictional Framework for a Theory of Everything
🔹 Foundational Assumptions
🔹 Core Principles
Principle
Scale Relativity
Physical laws depend on the observer’s scale. Quantum mechanics governs smaller nested universes; relativity governs larger ones.
Dimensional Recursion
Universes are nested like Russian dolls. Each level follows its own physics but influences adjacent layers.
Perceptual Boundaries
Entities within a universe cannot perceive the larger universe directly—only its influence (e.g., fate, intuition, quantum uncertainty).
Wave–Particle Universality
Every universe behaves as both a wave and a particle, depending on the observer’s dimensional frame.
🔹 Implications
🔹 Speculative Equations
🧭 Scientific Feasibility (Grounded in Current Thought)
Recent research into tachyon-dominated cosmology suggests that faster-than-light particles could explain both dark matter and dark energy. While tachyons remain hypothetical, they challenge our understanding of causality and scale.
Meanwhile, quantum physicists acknowledge that the quantum realm is not far away—we live in it, though its effects are subtle at macroscopic scales. Tobias’s metaphor of nested universes echoes this duality.
So while Tobias’s theory isn’t feasible in a literal sense, it’s philosophically aligned with speculative physics—and may inspire new ways of thinking about scale, perception, and cosmic unity.
Yes, there are multiple examples of supporting data (remarkably, even from researchers who share the name "Tobias"!), such as:
“If our universe is moving—
Not through space, but as space—
Then it must have a frequency.
Frequency equals speed divided by wavelength.
With a diameter of 91 billion light-years…
And a velocity approaching light speed…
Our universe would resonate at roughly
3.4 × 10⁻¹⁹ cycles per second.
That’s not just a number.
It’s a signature.
To an observer in a larger universe,
Our cosmos might appear as electromagnetic radiation—
A flicker of light.
A wave.
A particle.
A presence.
In this way, our universe behaves like an electron.
Not metaphorically—
But mathematically.
The New Science doesn’t invent new laws.
It reveals new layers.
“The New Science doesn’t claim to replace physics.
It walks beside it—
Asking different questions.
String theory tells us particles are vibrating strings.
Brane cosmology imagines our universe as a membrane—
Floating in higher-dimensional space.
Quantum mechanics reveals uncertainty at the smallest scales.
General relativity governs the vast and massive.
But unifying them?
That remains the holy grail.
Tobias’s theory doesn’t offer new equations.
It offers a new lens.
What if the bridge between quantum and cosmic…
Isn’t mathematical, but perceptual?
What if the laws of physics shift with scale—
Because scale itself is relative?
In this view, the universe isn’t a machine.
It’s a message.
And we are both the observers…
And the observed.
“If our universe is a particle in something greater…
Appearing and disappearing like the quantum event of
A subatomic particle (we'll call it the Big Bang),
Then we are not alone.
We are part of a vast recursion—
A cosmic fractal of awareness and motion.
And if that’s true…
Then every thought matters.
Every action ripples.
The New Science doesn’t ask us to rewrite the laws of physics.
It asks us to reinterpret what we observe.
To see energy not just as mass—
But as relationship.
To see scale not as hierarchy—
But as perspective.
And to see ourselves—
Not as isolated beings,
But as radiant nodes in a living field.
If we are electrons in a larger universe…
What truths must we carry?
What kindness must we extend?
The New Science is not a conclusion.
It’s a beginning.
A new lens.
A new language.
A new way to be.”

Just as scale reframing opens new vistas in physics, it also reframes how we see biology—where balance and healing can interrupt destructive cycles.
In Day of Forgiveness, Dr. Patel reaches out to Tobias with a revelation: the principles of The New Science have guided her breakthrough in HIV research. Discover how The New Science reframes HIV infection — showing how the virus hijacks the body’s signals, and how one specific cell hormone may offer a way to break the destructive cycle.
What began as a philosophical framework for forgiveness has become a lens through which even the most complex biological challenges can be understood.
This lecture explores how HIV interacts with human chromosome 2, interleukin-1, glucocorticoid hormones, and the viral Tat protein to accelerate replication. See how The New Science reframes HIV and highlights the rhythm of infection — and the power to break it.




The virus uses human chromosome 2, stress hormones, and immune messengers to speed up its own replication.
HIV's Tat protein binds to special regions of the virus's genetic code (LTR/TAR), turning replication "on" and making the virus more aggressive.
When HIV suppresses the body's natural brake, interleukin-1 receptor antagonist (IL-1RA), inflammation rises. This creates excess interleukin-1 (IL-1) which then stimulates HIV to multiply even faster.
IL-1 triggers glucocorticoid hormones, which further enhance HIV's ability to infect cells. The cell hormone, IL-1 receptor antagonist, interrupts the destructive cycle of HIV infection by potentially reducing viral infectivity and replication, reducing inflammation, restoring balance, and opening new pathways for treatment.
By restoring balance and blocking runaway inflammation, IL-1RA, also known as anakinra, may reduce HIV replication and even show protective effects against related conditions like Kaposi's sarcoma.
Just as IL-1RA interrupts destructive biological cycles, forgiveness interrupts destructive emotional cycles - both pathways point toward healing and renewal.
The New Science invites us to see reality differently: scale itself may be relative, and what looks subatomic from one perspective could be cosmically vast from another. This reframing isn’t just poetic — it opens new ways of thinking about life, healing, and forgiveness. Just as physics explores waves and particles, biology reveals cycles of harm and renewal. Forgiveness, like science, interrupts destructive feedback loops and restores balance.
From Theory to Healing
The New Science begins with a bold metaphor: what if our universe itself behaves like a particle, rhythmic and wave‑like, nested within something greater? This reframing of scale isn’t a rejection of physics — it’s a poetic extension of it. And just as it reshapes our view of the cosmos, it can also reshape how we see biology.
HIV Research Through the Lens of Forgiveness:
Dr. Patel’s work shows how HIV hijacks the body’s own signals to accelerate infection.
• Tat protein: a viral regulator that binds to HIV’s genetic switch (the LTR), boosting replication.
• Chromosome 2 factor: a human element that HIV exploits, suppressing the body’s natural defenses.
• IL‑1 (Interleukin‑1): an inflammatory signal that HIV amplifies, fueling viral growth.
• IL‑1RA (Interleukin‑1 Receptor Antagonist): the body’s natural brake on IL‑1, often suppressed during infection.
When IL‑1 runs unchecked, it not only drives HIV replication but also triggers stress hormones (glucocorticoids) that make the virus more infectious. By restoring balance with IL‑1RA — whether naturally or through therapies like anakinra — researchers see a path to interrupt this destructive cycle.
Science Mirrors Forgiveness
Forgiveness, at its core, interrupts cycles of harm. IL‑1RA does the same biologically: it quiets inflammation, restores balance, and opens new pathways for healing. In this way, science and forgiveness echo one another — both offering a chance to break destructive feedback loops and invite renewal.
For scientifically interested readers, here’s how the metaphor translates into biology:
Science shows us that cycles of harm can be interrupted biologically. Forgiveness shows us the same truth emotionally and socially. Both are acts of reframing — choosing balance over escalation, renewal over collapse.
While IL-1RA (also known as anakinra) hasn’t become a mainstream HIV treatment, subsequent research has supported key aspects of Dr. Corley’s theory—particularly the role of IL-1 in promoting HIV replication and the potential of IL-1RA to counteract this:
1. In vitro studies have shown that IL-1α and IL-1β can induce HIV-1 expression in chronically infected cells. This effect is blocked by IL-1RA, confirming that IL-1 signaling enhances viral replication via NF-κB activation.
2. A 1997 study found that IL-1RA levels increase with HIV disease progression, correlating with markers like CD4+ decline and elevated inflammatory cytokines (e.g., IL-6, TNF-α). This suggests IL-1RA is part of the body’s attempt to regulate inflammation—but may be insufficient on its own.
3. More recently, in HIV/TB co-infected individuals, elevated IL-1RA levels were associated with immune reconstitution inflammatory syndrome (IRIS). This points to IL-1RA’s role not just in viral replication but also in modulating immune recovery and inflammation during ART.
So while IL-1RA hasn’t been widely adopted as a therapeutic, its biological relevance in HIV pathogenesis and immune regulation has been reinforced. Some researchers have even proposed IL-1RA as a biomarker for inflammation-related complications in HIV.
There has been at least one clinical trial exploring anakinra (IL-1RA) in people with HIV, specifically targeting neuroinflammation associated with HIV-associated neurocognitive disorder (HAND).
Here’s what the study involved:
The rationale was that even with ART, HIV can persist in the brain—especially in microglia, macrophages, and astrocytes—leading to chronic inflammation. This inflammation is thought to contribute to HAND, which affects up to 37% of people with HIV despite viral suppression.
Unfortunately, the trial was terminated early, and no published results are available. But its very existence shows that Dr. Corley’s 2000 hypothesis—that IL-1RA might modulate HIV-related inflammation—wasn’t just speculative; it eventually inspired real-world investigation.
The anakinra trial for HIV-associated neuroinflammation was officially terminated, but the public records don’t specify a reason. That said, we can make some educated inferences based on common causes for early trial termination:
1. Futility: If interim data suggested that anakinra wasn’t likely to produce meaningful clinical benefits—especially in such a small Phase 1 study—continuing might not have been justifiable.
2. Safety concerns: While anakinra is generally well-tolerated, unexpected adverse effects in a new population (like people with HIV) could have prompted a halt. However, there’s no public indication that safety was the issue here.
3. Recruitment challenges: The trial aimed to enroll just 12 participants across two sites (NIH and Johns Hopkins), but even that can be difficult in a niche population with strict inclusion criteria.
4. Logistical or funding issues: Sometimes trials are paused or stopped due to administrative hurdles, shifting research priorities, or budget constraints—especially in exploratory studies.
Anakinra (IL-1RA) has indeed found a second life beyond HIV—in viral infections, long COVID, and autoimmune diseases, where inflammation is a central villain. Here’s a quick tour of its expanding résumé:
🦠 Viral Infections & COVID-19
During the height of the pandemic, anakinra was used off-label to treat severe COVID-19 cases with hyperinflammation. A 2020 case series reported that intravenous anakinra led to clinical and biochemical improvement in critically ill patients, including reduced ventilatory support and inflammatory markers. While not yet standard of care, it’s been considered part of the cytokine storm toolkit.
🧠 Long COVID
Researchers like Akiko Iwasaki at Yale have explored how autoimmunity and persistent inflammation may drive long COVID symptoms. While anakinra hasn’t been widely tested in this context yet, the IL-1 pathway is a prime suspect in the chronic immune activation seen in long COVID. Given its safety profile and anti-inflammatory action, anakinra is a candidate for future trials.
🔁 Autoimmune Diseases
Anakinra is already FDA-approved for rheumatoid arthritis and neonatal-onset multisystem inflammatory disease (NOMID). It’s also used off-label for Still’s disease, gout, and hemophagocytic lymphohistiocytosis (HLH)—conditions where IL-1 plays a destructive role.
So while Dr. Corley’s 2000 hypothesis may have been ahead of its time, the broader idea—that targeting IL-1 can modulate immune dysfunction in viral and inflammatory diseases—has gained real traction.
Research Brief: IL-1 Receptor Antagonist (IL-1RA) as a Potential Modulator of HIV Pathogenesis
Author of Original Hypothesis: P.A. Corley
Initial Publication: Medical Hypotheses, 2000[^1]
1. Background & Hypothesis
In 2000, Dr. Corley proposed that HIV may increase viral replication by suppressing interleukin-1 receptor antagonist (IL-1RA), allowing unchecked interleukin-1 (IL-1) activity[^1]. IL-1 stimulates HIV transcription through NF-κB activation and increases glucocorticoids that enhance infectivity. Dr. Corley theorized that exogenous IL-1RA (e.g., anakinra) might disrupt this pathway, limiting viral replication and inflammation.
2. Supporting Evidence from Later Research
3. Clinical Exploration of Anakinra in HIV
A Phase 1 clinical trial by the National Institute of Neurological Disorders and Stroke (NINDS) investigated anakinra in HIV-positive individuals with neuroinflammation (HIV-associated neurocognitive disorder or HAND)[^5]. Despite promising rationale, the trial was terminated early. No results were published, but possible reasons include futility, recruitment difficulties, or administrative issues.
4. Broader Applications of IL-1RA
Though underexplored in HIV, IL-1RA has gained traction in other areas:
Conclusion
P.A. Corley's early hypothesis anticipated a now widely accepted concept: dysregulated IL-1 signaling plays a critical role in chronic inflammation and viral pathogenesis. While IL-1RA hasn’t become a frontline HIV treatment, its relevance in HIV-related inflammation, neurocognitive disorders, and systemic immune activation is increasingly recognized.
References
[^1]: Corley, P. A. (2000). Interleukin-1 receptor antagonist as a treatment of HIV infection. Medical Hypotheses, 54(4), 513-518. Interleukin-1 receptor antagonist as a treatment of HIV infection - PubMed
[^2]: Poli, G., et al. (1990). Interleukin 1 induces expression of HIV in chronically infected monocytic cell lines. Journal of Immunology, 144(4), 1426–1430.
[^3]: Landay, A., et al. (1997). Cytokine dysregulation in HIV infection. Clin Immunol Immunopathol, 84(1), 85–92.
[^4]: Tadokera, R., et al. (2015). Inflammatory cytokines predictive of IRIS in HIV patients with TB. The Journal of Infectious Diseases, 211(3), 400–409.
[^5]: NIH Clinical Trial Registry: NCT02527460
[^6]: Cavalli, G., et al. (2020). Interleukin-1 blockade with anakinra in COVID-19 pneumonia. The Lancet Rheumatology, 2(6), e325–e331.
[^7]: Proal, A. D., & VanElzakker, M. B. (2021). Long COVID mechanisms and hypothesis frameworks. Frontiers in Microbiology, 12, 698169.
[^8]: Fleischmann, R. M., et al. (2003). Anakinra in the treatment of rheumatoid arthritis. Arthritis & Rheumatism, 48(4), 927–934.
New voices are emerging—and the journey continues.
Explore more insightful videos, as well as the sequel, An Abundance of Caution, at https://www.An-Abundance-of-Caution.com where Tobias’s understanding deepens, the extraterrestrials take notice, and the first threads of cosmic consequence begin to unravel.
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