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A Physicist's Perspective on Metabolic Rejuvenation After 50
Banerjee S.. Preprints.org, 2026-09-09
Topic: Gut, metabolism and diet
Chronic metabolic diseases, including Type 2 Diabetes, hypertension, non-alcoholic fatty liver disease (NAFLD), prostate enlargement, musculoskeletal joint friction, cardiac arrhythmias, neurodegenerative waste accumulation (Alzheimer's), and elevated intraocular hydraulic pressure (glaucoma), are frequently treated as distinct, unavoidable consequences of chronological aging. However, from a systems engineering and thermodynamic perspective, the human body is an open system whose homeostatic equilibrium is dictated entirely by its input parameters. This article analyses the mechanical and biochemical pathways of human nutrition, specifically examining how dietary choices past the age of 50 modulate our master hormonal control valve: insulin. By evaluating comparative gastrointestinal architecture, this paper establishes that our physiology is evolutionarily optimized for nutrient-dense, low-entropy structural proteins and stable lipids, rather than volatile carbohydrate loads. Chronic carbohydrate influx triggers signal attenuation (insulin resistance), initiating a destructive positive feedback loop. Our liver acts as an emergency overflow reservoir, converting excess glucose into triglycerides, leading to visceral adiposity, which systematically suffocates our pancreas and gallbladder. This metabolic backlog degrades cardiovascular fluid dynamics via the suppression of endothelial nitric oxide and the permanent activation of epithelial sodium channels (ENaC) in the kidneys, causing chronic hypertension. Furthermore, this systemic signal failure acts as a potent growth accelerator in the prostate matrix, starves chondrocytes and spinal discs of nutrients to trigger musculoskeletal wear, generates disruptive electrophysiological noise in the cardiac grid, induces central nervous system energy failure (metabolic crisis) by overwhelming amyloid-clearing enzymes (amyloid is an abnormal misfolded protein), and clogs the ocular trabecular filtration sieve (optic nerve damage in glaucoma). To reverse this systemic decay, this paper outlines a practical framework utilizing the physics of gastric emptying, circadian chrononutrition, and zero-input windows (16:8 intermittent fasting). These targeted interventions leverage hormetic stress and mitophagy to flush out accumulated oxidized lipids, eliminate senescent cells, and restore high-yield mitochondrial efficiency, providing a hypothesis-driven framework for senior metabolic rejuvenation.
Key findings
- Our liver acts as an emergency overflow reservoir, converting excess glucose into triglycerides, leading to visceral adiposity, which systematically suffocates our pancreas and gallbladder.
- This metabolic backlog degrades cardiovascular fluid dynamics via the suppression of endothelial nitric oxide and the permanent activation of epithelial sodium channels (ENaC) in the kidneys, causing chronic hypertension.
- Furthermore, this systemic signal failure acts as a potent growth accelerator in the prostate matrix, starves chondrocytes and spinal discs of nutrients to trigger musculoskeletal wear, generates disruptive electrophysiological noise in the cardiac grid, induces central nervous system energy failure (metabolic crisis) by overwhelming amyloid-clearing enzymes (amyloid is an abnormal misfolded protein), and clogs the ocular trabecular filtration sieve (optic nerve damage in glaucoma).
- To reverse this systemic decay, this paper outlines a practical framework utilizing the physics of gastric emptying, circadian chrononutrition, and zero-input windows (16:8 intermittent fasting).
- These targeted interventions leverage hormetic stress and mitophagy to flush out accumulated oxidized lipids, eliminate senescent cells, and restore high-yield mitochondrial efficiency, providing a hypothesis-driven framework for senior metabolic rejuvenation.
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Study details
- Evidence strengthLow
How this study scored 16/100
Preprint — not yet peer-reviewed. It scored 21 on the same rubric, but non-peer-reviewed sources are capped at 16, so it shows as 16. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 13 of the 62 points we could judge it on, which is 21 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 2 / 10 | Tier 4 — not a peer-reviewed journal (Preprints.org) |
| Journal's citation record | 0 / 4 | Not a journal article, so the journal's record does not count |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 4 / 10 | Preprint — not yet peer-reviewed. Hosted on a preprint server. |
| How recent | 5 / 5 | 2026 — within 1 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 1 / 2 | Not in PubMed, but has a DOI |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 13 / 62 | Scored on 12 of 20 parts. We have no data for the rest, so they are left out: 13 of the 62 points we could judge it on is 21 out of 100. |
| Total | 21 / 100 | Capped to 16 because this is not a peer-reviewed article. |
What each of these 20 components measures, and what this score is not →
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Banerjee, S. (2026). A Physicist's Perspective on Metabolic Rejuvenation After 50. Preprints.org. https://doi.org/10.20944/preprints202609.0698.v1
Vancouver
Banerjee S. A Physicist's Perspective on Metabolic Rejuvenation After 50. Preprints.org. 2026. doi:10.20944/preprints202609.0698.v1.
BibTeX
@article{banerjee2026-a8f0164f,
author = {Banerjee, S.},
title = {{A Physicist's Perspective on Metabolic Rejuvenation After 50}},
journal = {Preprints.org},
year = {2026},
doi = {10.20944/preprints202609.0698.v1},
url = {https://doi.org/10.20944/preprints202609.0698.v1}
}
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