Latest / Peptides Weekly / Ep 5: Three to four extra rare vision-loss cases per ten thousand showed up in an observational…

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Ep 5: Three to four extra rare vision-loss cases per ten thousand showed up in an observational… · Peptides Weekly

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  Three to four extra rare vision-loss cases per 10,000 showed up in an observational glp-1 study. This is peptides weekly, episode five, education and evidence, never-dosing advice. Rutgers researchers followed adults in the United States who had type 2 diabetes and had just begun treatment. ScienceDailyNUA.News both described the paper in annals of internal medicine. The comparison is observational. People starting a glp-1 receptor agonist had a higher chance of a schematic optic neuropathy.
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  which happens when blood flow to the optic nerve drops.
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  Chintan Dave at Rutgers said the condition matters
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  because vision can fail suddenly,
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  even though the added risk is small.
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  Semaglutide, sold as ozempic and wagovi,
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  and tear-zepatide, sold as mongaro and zepbound,
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  are approved drugs used for blood sugar and body weight.
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  The class can also lower the risk of some heart and kidney problems.
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  On estimates cited by UA.News,
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  more than 80% of these optic nerve cases are the non-artoritic anterior form.
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  They showed up more often in men and in people from 50 to 65.
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  The authors said other illnesses could explain the pattern, so the link is not
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  proof the drugs damaged the nerve. They also said a sudden change in sight
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  should not wait on an eye exam. On October 8th, this show was on nails and hair with
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  these medicines. Today's paper is a different measured risk in medical records,
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  not a repeat of that side-effect list. Researchers at UC Santa Cruz are pointing at a peptide called P3.
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  Science daily says it had been treated as harmless for years. This is not a study in people.
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  The report says P3 can form harmful looking clumps even faster than amyloid beta, and that it may injure brain cells.
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  Amyloid beta has been the main Alzheimer's target for decades, and many of those drugs disappointed.
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  This write-up puts P3 next to that peptide as another possible contributor without offering
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  a treatment result.
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  Verdiva has stopped a mid-stage study of an oral GLP1.
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  BioSpace says the company pointed to market evolution.
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  That is a decision about an investigational program.
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  It is not a published trial result, and it is not an approval.
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  The report does not include efficacy or safety figures from the study that ended.
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  Medical Daily says the FDA is weighing wider access to peptides, while adverse event reports
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  and two intubations in Las Vegas sharpen the safety questions.
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  The piece is tied to BPC157.
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  That is news about harm reports in policy, not a clinical trial.
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  Products sold outside ordinary drug controls can also differ in purity and contamination.
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  Buchanan Ingersol and Rooney describes a temporary FDA enforcement reprieve on peptide compounding,
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  and what it could mean for pharmacies.
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  A policy pause is not evidence
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  that a compounded peptide works or is safe.
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  A compounded preparation is not the same thing
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  as a fully reviewed approved medicine.
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  A physician at MU health care
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  is warning people away from unregulated peptides.
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  KOMU eight reported the warning.
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  That is clinical commentary, not a new experiment.
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  Peptides sold without regulatory controls
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  can differ in purity and contamination
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  from anything studied under a trial protocol.
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  BPC-157, the compound in this week's spotlight, is 15 amino acids long, a fragment of a body
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  protection peptide isolated from human gastric juice.
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  The groups that study it treated as a healing signal that also touches nitric oxide.
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  The gas vessels used to manage blood flow.
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  In a 1997 rat paper, stomach tissue homogenates made nitric oxide when the peptide was added,
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  at a level comparable to the amino acid L-arginine. L-name, a blocker of the enzyme that makes nitric oxide,
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  stopped the L-arginine effect and did not stop the peptide effect. Putting the peptide and L-arginine
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  together blunted nitric oxide synthesis in that dish. In the same rat work, the peptide reduced alcohol
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  injury to the stomach lining and changed blood pressure responses to L-name and L-arginine
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  in a pattern that was not a copy of L. Arginine alone.
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  A 2014 review reads this as the peptide joining the nitric oxide response after a vessel is damaged.
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  Depending on the injury model, the authors describe less clotting or less bleeding and fewer platelets.
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  That review also says the peptide turns on the genes EGR1 and NAB2.
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  A 2018 review sets it beside EGF, FGF, and VGF, and says its own angiogenic effect appears
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  in the healing models those authors surveyed. The tendon evidence is rat tissue on a bench,
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  not patients. Explans grew out faster. An MTT assay showed no direct boost in fibroblast
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  proliferation. Cells given the peptide survived hydrogen peroxide stress better. They migrated more
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  as the amount rose, spread faster on dishes, and built F-Actin.
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  Phosphorylation of FAK and Paxilin rose with the amount of peptide, while the total amount
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  of those proteins stayed the same.
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  The author's Thai Outgrowth, Stress Survival, and Migration to that FAK Paxilin Path.
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  A 2026 critical review, with searches through the 24th of June that year, looks at rodent
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  ischemia-reperfusion models.
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  angles. Across those papers, the peptide was associated with less oxidative injury, shifts
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  in nitric oxide vessel responses, and lower inflammatory and apoptotic markers. The same
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  review describes changes in VEGF R2, AKT, and E&O signaling. Reported settings include
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  leg muscle ischemia reperfusion, distant organs after a limb injury, the hippocampus, intestine
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  and colon and a hepatic pringle maneuver.
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  The reviewers did not pool the numbers.
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  Organs, roots, timing, and outcomes were too mixed.
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  Follow-up was often short.
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  Many designs used a single dose, and risk of bias was incompletely described.
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  They also say blocking a major vessel is not the same experiment as classic organ ischemia
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  reperfusion.
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  A 2018 review claims the peptide, given alone, was consistently effective in acute and chronic
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  injury models of esophagus, stomach, duodenum, and lower gut, by injection into the abdomen,
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  by mouth, or locally. That review also says the same experimental regimens improve tendon,
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  ligament, and bone healing in the studies surveyed. Those are animal models summarized by
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  reviewers, not outcomes measured in patients. A 2013 review calls it proven safe in inflammatory
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  bowel disease trials coded PL-10, PL-D-116, and PL-14736, and in wound healing
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  and says no toxicity was reported, and a lethal dose was never reached.
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  That abstract does not say how many people were enrolled or what the trials measured
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  beyond that safety claim.
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  The same review argues the peptide can counter several NSAID injuries in gut, liver, and brain,
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  plane, plus effects on bleeding and clots, from the experimental work the authors assemble.
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  The 2014 review says turning nitric oxide modulation into better clinical performance remains
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  to be determined.
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  A separate 2026 material's paper built a kytosan hydrogel carrying the peptide.
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  Infrared spectroscopy showed hydrogen bonds between the peptide and the kytosan backbone,
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  and the gel was porous.
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  Water vapor transmission was about 2,270 grams per square meter per day.
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  With a spread of 35, encapsulation was 98.9%, plus or minus 0.8, and 81.2%, plus or
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  minus 2.9, came out within 24 hours.
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  Inhibition reached 45.9% against E. coli and 65% against staff aureus.
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  Himalosus stayed under 5%, which the authors read as acceptable hemocompatibility in that
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  lab test, not as a human safety result.
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  None of these abstracts stayed in approval, an indication, or a regulator's decision.
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  Name trial codes are not the same thing as a licensed medicine.
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  Older reviews describe a wide pre-clinical safety margin.
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  That is not a finished human safety record, and it says nothing about purity when a peptide
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  is sold outside a controlled study.
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  One thing worth knowing is that a record's link between starting a GLP1 medicine, and
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  a rare optic nerve injury is a signal, not proof the drug caused it.
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  Another is that a rare association can still matter when millions of people take a drug,
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  which is why the authors called the finding clinically important while still calling
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  the absolute risk low.
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  A third is that ending a mid-stage oral GLP1 study is a development choice about an
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  investigational peptide, not a verdict that the class failed or succeeded in people.
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  That's peptides weekly.
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  This show is education, not medical advice.
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  Talk to your own clinician before acting on anything you heard.
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  I'm Patrick and Vancouver.
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  See you next week.
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  is waiting for you.
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  This episode used AI voice synthesis of my voice.
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  Editorial selection and analysis are my own.