More than $21 billion has flowed into longevity. The bigger question now is what actually holds up. Today, Super Human Network and @BCG launch The Longevity Review 2026, a new annual benchmark built to give the field a clearer reference point. The report looks at what research supports, what remains unproven, where capital is flowing, and what people around the world actually understand and want. It combines global research and investment data, BCG consumer research across 19 countries, and perspectives from 14 leading experts, including @davidasinclair, @aubreydegrey, @daveasprey, Andrea Maier and Kayla Barnes-Lentz. So where does longevity actually stand in 2026? Download The Longevity Review 2026 at longevityannual.com.

This machine makes your muscles work harder without simply adding more reps. At Super Human Summit 2026, we caught up with the @technogym team to see its Biostrength system in action. In this demo, he pulls 62 kg, then resists 81 kg on the return using Eccentric Overload. The idea is that instead of keeping resistance the same through the entire rep, the machine increases the load during the eccentric phase, when your muscles are capable of handling more. It’s a smart example of where strength training is heading: more personalized, more precise, and built around how the body actually moves.

Researchers just reversed a type of protein damage that builds up as we age. Researchers from Revel Pharmaceuticals, Calico Life Sciences and the University of Colorado engineered an enzyme called CMLase to remove CML — a type of age-related chemical damage that accumulates on proteins over decades and is linked with inflammation and tissue dysfunction. To build it, the team screened and evolved more than 500 million enzyme variants until they created one capable of removing CML and restoring the protein’s original lysine. Then they tested it on actual aged human tissue. CMLase reduced CML by more than 70% in elderly arterial tissue and more than 55% in older human skin. It also removed accumulated damage from proteins taken from a 64-year-old human lens. That’s important because most approaches to this type of damage have focused on preventing more from forming. This study suggests that some damage already accumulated over decades may actually be repairable. There’s a huge caveat: these experiments were performed outside the body, not in living people. We don’t yet know whether CMLase can be safely delivered into humans or whether removing this damage will improve health or lifespan. But as a proof of concept, it challenges a pretty fundamental assumption about aging: some molecular damage we thought was permanent may not have to be. Study: Trabosh et al., Nature Communications (2026).

Microplastics were detected in the coronary blood of 84% of heart attack patients in a new study. Researchers in Italy studied 61 people undergoing coronary angiography, including 19 patients experiencing a STEMI heart attack, 20 with chronic coronary disease, and 22 with normal coronary arteries. Micro- and nanoplastics were found in: - 84% of heart attack patients - 40% of chronic coronary disease patients - 32% of people with normal coronary arteries Heart attack patients also had higher concentrations and a greater variety of plastic particles in their blood. Polyethylene was the most commonly detected polymer. Researchers found that concentrations were actually higher in blood taken from the coronary circulation — the blood supply of the heart — than in peripheral blood. Smoking and higher exposure to fine-particle air pollution were also associated with greater detection of microplastics, while the heart attack group showed higher levels of inflammatory markers. But there’s an important limitation: this was a small, cross-sectional study, so it cannot show that microplastics caused the heart attacks. What it does show is that these particles are reaching the circulation around the heart — and researchers now want to understand whether they could play a role in inflammation and cardiovascular disease. Study: Paolisso et al., European Heart Journal (2026).

How long could we theoretically live if diseases and aging damage were eliminated? Their answer: a median lifespan of roughly 146–194 years. Researchers at the Skolkovo Institute of Science and Technology and the Artificial Intelligence Research Institute focused on somatic mutations — random DNA errors that build up inside our cells over time. Without that genetic damage, one version of their model produced a median lifespan of 1,759 years. But once somatic mutations were added back in, lifespan dropped dramatically. The biggest bottlenecks were the brain and heart, where many important cells divide rarely or not at all, allowing DNA damage to keep accumulating. That doesn’t mean humans can currently live to 194, or that 194 is a proven biological limit. It suggests that even if medicine someday controls most age-related disease, repairing DNA damage in long-lived cells may become one of the next major barriers to extreme longevity. Study: Efimov et al., Somatic mutations impose an entropic upper bound on human lifespan, npj Aging (2026).