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PreprintCC BYbioRxiv

Can the Human Plastisphere Account for the Rise of Type 1 Diabetes: A Computational Molecular Mimicry Study

  1. 1University of Utah

Abstract

An increased incidence of childhood type 1 diabetes mellitus (T1DM) has been widely documented, but its pathophysiological origins are poorly understood. The post-World War II expansion of the plastics industry in the United States and elsewhere coincides with a marked increase in T1DM incidence; however, no pathophysiological mechanism has been proposed that could justify such a temporal correlation. Here, we leverage recent advances in artificial intelligence and protein structure prediction and binding to show that molecular mimicry is a plausible pathophysiological mechanism for plastic fragments to induce onset of T1DM for individuals with certain HLA haplotypes.

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BibTeX
@misc{facelli2026human,
  title = {{Can the Human Plastisphere Account for the Rise of Type 1 Diabetes: A Computational Molecular Mimicry Study}},
  author = {J. Facelli and M. jones and S. Mistry and R. Gouripeddi},
  howpublished = {bioRxiv},
  year = {2026},
  month = nov,
  doi = {10.64898/2026.11.02.763715},
  url = {https://www.biorxiv.org/content/10.64898/2026.11.02.763715v1},
  note = {CC BY},
}
RIS
TY  - UNPB
TI  - Can the Human Plastisphere Account for the Rise of Type 1 Diabetes: A Computational Molecular Mimicry Study
AU  - J. Facelli
AU  - M. jones
AU  - S. Mistry
AU  - R. Gouripeddi
PY  - 2026
DA  - 2026/11/02
PB  - bioRxiv
DO  - 10.64898/2026.11.02.763715
UR  - https://www.biorxiv.org/content/10.64898/2026.11.02.763715v1
AB  - An increased incidence of childhood type 1 diabetes mellitus (T1DM) has been widely documented, but its pathophysiological origins are poorly understood. The post-World War II expansion of the plastics industry in the United States and elsewhere coincides with a marked increase in T1DM incidence; however, no pathophysiological mechanism has been proposed that could justify such a temporal correlation. Here, we leverage recent advances in artificial intelligence and protein structure prediction and binding to show that molecular mimicry is a plausible pathophysiological mechanism for plastic fragments to induce onset of T1DM for individuals with certain HLA haplotypes.
ER  -