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2025
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| Acceso en línea: | https://doi.org/10.5281/zenodo.17121897 |
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| _version_ | 1866902276881252352 |
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| author | Mitchell, D. B. |
| author_facet | Mitchell, D. B. |
| contents | <p>Lithium, long regarded as a paradoxical element, remains suspended between three identities: contaminant, drug, and nutrient. At pharmacological doses it is a cornerstone therapy for mood disorders, yet at trace levels in drinking water it is consistently associated with protection against dementia and suicide. Despite decades of evidence, lithium is not recognized as essential, and its biological role remains undefined. We propose a unifying resolution: lithium is not primarily a biochemical co-factor but a biophysical stabilizer for the cell's predictive hardware. Within the Computational Organellopathy (CO) framework, which identifies the ancient cellular vault as a subcellular computer, we advance the Computational Stabilizer Hypothesis: trace lithium is uniquely required to maintain the conformational integrity of vault RNA (vRNA)—the "geome"—whose folding encodes the vault's predictive software. Deficiency therefore constitutes a fundamental hardware fault, destabilizing the vRNA landscape and precipitating systemic computational collapse. This collapse manifests biochemically through critical downstream pathways, most notably runaway GSK3β activation and autophagy failure—two hallmarks of lithium biology previously lacking a common origin.</p> <p>By reframing lithium's role as physical rather than metabolic, this model provides a testable framework for resolving four long-standing paradoxes of function, scale, evidence, and policy. It predicts that a modern convergence of pressures—including reduced intake from depleted water supplies, accelerated excretion from Western diets, and novel biophysical sequestration by the alarming internal burden of microplastics—is driving widespread insufficiency. The ability of this mechanistic account to resolve the lithium paradox offers powerful corroborating evidence for the CO framework and reveals that the biophysical integrity of subcellular computation is a fundamental determinant of health—one now directly threatened by the modern chemical exposome.</p> |
| format | Recurso digital |
| id | zenodo_https___doi_org_10_5281_zenodo_17121897 |
| institution | Zenodo |
| language | |
| publishDate | 2025 |
| publisher | Zenodo |
| record_format | zenodo |
| spellingShingle | Lithium is a Computational Stabilizer: A Biophysical Resolution to the Lithium Paradox in Health and Disease Mitchell, D. B. Lithium Computational Organellopathy Cellular Vault Free Energy Principle (FEP) Cancer Alzheimer Disease Parkinson Disease Depression Autism Spectrum Disorder Metabolic Syndrome Vault RNA (vRNA) RNA Biology Microplastics Neurodegenerative Diseases Theoretical Biology Pathology Oncology Psychiatry Systems Biology Computational Biology Biophysics Public Health Nutritional Sciences Quantum Biology <p>Lithium, long regarded as a paradoxical element, remains suspended between three identities: contaminant, drug, and nutrient. At pharmacological doses it is a cornerstone therapy for mood disorders, yet at trace levels in drinking water it is consistently associated with protection against dementia and suicide. Despite decades of evidence, lithium is not recognized as essential, and its biological role remains undefined. We propose a unifying resolution: lithium is not primarily a biochemical co-factor but a biophysical stabilizer for the cell's predictive hardware. Within the Computational Organellopathy (CO) framework, which identifies the ancient cellular vault as a subcellular computer, we advance the Computational Stabilizer Hypothesis: trace lithium is uniquely required to maintain the conformational integrity of vault RNA (vRNA)—the "geome"—whose folding encodes the vault's predictive software. Deficiency therefore constitutes a fundamental hardware fault, destabilizing the vRNA landscape and precipitating systemic computational collapse. This collapse manifests biochemically through critical downstream pathways, most notably runaway GSK3β activation and autophagy failure—two hallmarks of lithium biology previously lacking a common origin.</p> <p>By reframing lithium's role as physical rather than metabolic, this model provides a testable framework for resolving four long-standing paradoxes of function, scale, evidence, and policy. It predicts that a modern convergence of pressures—including reduced intake from depleted water supplies, accelerated excretion from Western diets, and novel biophysical sequestration by the alarming internal burden of microplastics—is driving widespread insufficiency. The ability of this mechanistic account to resolve the lithium paradox offers powerful corroborating evidence for the CO framework and reveals that the biophysical integrity of subcellular computation is a fundamental determinant of health—one now directly threatened by the modern chemical exposome.</p> |
| title | Lithium is a Computational Stabilizer: A Biophysical Resolution to the Lithium Paradox in Health and Disease |
| topic | Lithium Computational Organellopathy Cellular Vault Free Energy Principle (FEP) Cancer Alzheimer Disease Parkinson Disease Depression Autism Spectrum Disorder Metabolic Syndrome Vault RNA (vRNA) RNA Biology Microplastics Neurodegenerative Diseases Theoretical Biology Pathology Oncology Psychiatry Systems Biology Computational Biology Biophysics Public Health Nutritional Sciences Quantum Biology |
| url | https://doi.org/10.5281/zenodo.17121897 |