Plasma Exchange and Biological Age, Amylin Analogs, and Lab-Grown Islet Cells

Your blood is roughly half cells and half plasma, the straw-colored fluid that carries proteins, hormones, and inflammatory signals. As people age, plasma accumulates molecules linked to inflammation and tissue damage. The theory behind therapeutic plasma exchange is simple: swap out the old plasma and you dilute those signals. Animal work over the past decade, including blood-swapping experiments in mice, gave the idea some credibility.

Researchers led by teams at the Buck Institute and the University of California ran what appears to be the first placebo-controlled human test aimed at aging rather than disease. Healthy adults over 50 were assigned to monthly TPE, twice-monthly TPE, twice-monthly TPE plus intravenous immunoglobulin (IVIG, a concentrated antibody preparation), or a placebo procedure. The team then measured biological age using dozens of epigenetic clocks alongside protein and metabolite profiling. Published in Aging Cell in May 2025, the analysis found that TPE alone lowered biological age by about 1.3 years on average, while TPE plus IVIG lowered it by about 2.6 years. Fifteen separate epigenetic clocks moved in the rejuvenating direction versus placebo. Across 240 procedures there was one mild allergic reaction and no serious safety signals.

Here is the honest caveat. Epigenetic clocks are statistical models trained to predict chronological age from chemical marks on DNA. They correlate with health, but shifting a clock reading is not the same as extending healthy life. The trial was small, ran for months rather than years, and measured no clinical endpoints such as strength, cognition, or disease incidence. TPE is also an invasive procedure that costs thousands of dollars per session and is not covered for this use. The result is genuinely interesting and worth following. It is not yet a reason to book an appointment.

Almost every weight-loss headline for the past three years has been about GLP-1 drugs. Amylin is a different hormone with a different job. Your pancreas releases it at the same time as insulin, and it slows how fast the stomach empties and signals fullness to the brainstem. Drug developers have spent years building longer-lasting versions of it, and 2026 is the year the data started arriving.

In March 2026, Zealand Pharma and Roche reported Phase 2 results for petrelintide, a once-weekly amylin analog, in 493 adults with overweight or obesity and an average BMI of 37. All five dose arms beat placebo. The best-performing arm reached about 10.7 percent average weight loss at 42 weeks compared with 1.7 percent on placebo. What drew attention was tolerability: in the most effective arm there was no vomiting reported and no participants stopped because of stomach side effects, with overall discontinuations for adverse events roughly matching placebo. Registrational Phase 3 trials were planned to begin in the second half of 2026. A second amylin analog, cagrilintide, has produced roughly 10.8 percent weight loss on its own in Phase 2 and about 22.7 percent at 68 weeks when combined with semaglutide.

For readers focused on healthspan rather than the scale, the question is body composition. Losing weight rapidly on any drug costs some muscle, and muscle is one of the strongest predictors of independence in later life. Early comparisons suggest amylin analogs may spare lean mass better than GLP-1 drugs, possibly because they work through a different brain circuit and cause less nausea-driven undereating. That claim is still preliminary. It rests on small studies and secondary measurements, not on a large trial designed to answer it. Watch for Phase 3 data that reports lean mass directly.

In type 1 diabetes the immune system destroys the beta cells inside the pancreas that produce insulin. Transplanting islet cells from deceased donors has worked for decades, but donor supply is tiny and results are inconsistent. The newer approach starts with stem cells and coaxes them, in a lab, into fully mature islet cells that sense glucose and release insulin on demand. That gives an essentially unlimited, standardized supply.

Zimislecel is the furthest along. In the FORWARD trial, the cells were infused into the portal vein leading to the liver, where they take up residence. Results published in mid-2025 covered 12 participants who received the full dose and had a year of follow-up. Ten of them no longer required any insulin. All 12 met the American Diabetes Association's targets for HbA1c under 7 percent and time-in-range above 70 percent, and severe low-blood-sugar episodes stopped. Blood tests confirmed the transplanted cells were making insulin themselves. The most common serious side effect was a drop in white blood cells, seen in three participants, which is attributable to the immune-suppressing regimen rather than the cells.

That regimen is the honest limitation. To keep the immune system from rejecting the transplanted cells, and from re-attacking them the way it attacked the original beta cells, recipients take ongoing immune suppression. That raises infection and cancer risk, which is why this is being studied first in people with severe, hard-to-control type 1 diabetes rather than everyone. Research groups are working on gene-edited cells designed to hide from the immune system, and on encapsulation devices that physically shield the cells. Regulatory submissions for zimislecel were expected during 2026. If it clears, it will be one of the first stem-cell-derived therapies to reach patients as an approved product rather than an experiment.