I attended this year’s Longevity Summit Dublin in June, hosted by the Longevity Escape Velocity (LEV) Foundation folk, but was so buried in work that there was no chance I would be able to take comprehensive notes for later formatting into a post here. Fortunately there are a good number of patient advocates in the community who can do just as good a job as I might, were I less encumbered, and thus Lifespan.io has published notes on some of the highlights from the conference.
The Longevity Summit Dublin is, if you like, the spiritual successor to the Strategies for Engineered Negligible Senescence (SENS) conference series of past years: scientists presenting novel research aimed at the goal of treating aging as a medical condition; biotech startups showcasing their programs of development relevant to the treatment of aging; patient advocates arguing for more funding and faster progress for all of the above. It is well worth attending if this is an area of research and development that interests you.
The first day began with a “pre-session” before the official opening, and the very first talk set an interesting tone. It was given by Michael Suk, the newly elected chair of the American Medical Association (AMA)’s Board of Trustees. The AMA is the biggest organization of medical doctors in the US, and having its leader talk at a longevity conference is an important event and an encouraging sign of our field inching closer to the mainstream. Suk, through a remote connection, praised the recent scientific advances that bring us closer to personalized medicine that would allow for continuing healthspan extension. “The work you do here,” he said, “has the potential to change lives, to offer hope where there is none, and to redefine the future of healthcare. Together, we are building a future where technology and compassion go hand in hand, where surgical care is not just about precision, but about people, and where the promise of a longer, healthier life is within reach for all.”
Aubrey de Grey welcomed the participants and expanded on longevity escape velocity (LEV), the concept he has been promoting for decades that gave the name to his foundation. LEV means buying time by eliminating age-related damage (another concept that de Grey pioneered and is now entering the mainstream): “If you take someone who is, let’s say, 60 years both chronologically and biologically, and you rejuvenate them reasonably well so that they’re back to being biologically 40, then they won’t be biologically 60 again until they’re 80.” However, some types of damage are harder to tackle, and they will continue to accumulate, but their effect will not be as devastating as today’s combined effects of all types of damage. Hopefully, during those 20 extra years of life, geroscientists “will have been continuing to improve this rejuvenation arsenal. The idea is that there’s some finite, in fact quite modest, minimum rate at which we need people like the people in this room to be improving the comprehensiveness of rejuvenation technologies in order to stay one step ahead of the problem.”
Revel Pharmaceuticals is one of those brave small companies to literally boldly go where no one has gone before: in this case, towards reversing the molecular damage produced by advanced glycation end products (AGEs). Like their name suggests, AGEs accumulate with age in blood and tissues, causing inflammation and the stiffening of the extracellular matrix by binding to molecules like collagen. Aaron Cravens, Revel’s CEO, told the audience that his company is after a specific AGE, carboxymethylysine (CML). It exists in two forms: a free form present in cells and a bound form that accumulates in the extracellular matrix (for instance, in arterial walls). “The body has no physiological means of removing this,” Cravens said. Revel built an enzyme engineering platform to develop bespoke enzymes. Currently, it focuses on removing the free-floating form of CML. It strongly contributes to inflammation, in particular by binding to the RAGE receptor and initiating inflammatory signaling.
Michael Ringel of the Boston Consulting Group talked about the recent trends in the longevity field. After decades of not taking geroscience seriously, there is apparently a growing understanding in society that investigating the biology of aging is the only way to ward off the economic threats of population aging and to meaningfully increase human lifespan. If we do nothing, global resources might be devastated by the need to care for the increasingly aged population, exacerbated by slumping birth rates. However, even a slight slowing of the rate of aging would bring unprecedented prosperity, adding hundreds of trillions of dollars to the global economy over the course of a decade.
The Rising Star Award this year went to Alexander Fedintsev from the Radical Life Extension Group. In his talk, Fedintsev proposed a new hallmark of aging: clonal hematopoiesis of indeterminate potential (CHIP). Clonal hematopoiesis is a condition in which a single hematopoietic stem cell (HSC) acquires genetic mutations that give it a growth advantage, allowing it to expand clonally within the bone marrow. This results in a significant proportion of blood cells being derived from this single mutated stem cell rather than from a diverse population of HSCs. Currently, we don’t have good tools to combat CHIP. However, prolonged inhibition of the pro-inflammatory cytokine IL-6 has shown some promise, including in non-human primates. Answering a question about how safe lifelong IL-6 inhibition is, Fedintsev noted that rheumatoid arthritis patients receive such therapy, which only causes a slight increase in infections but is associated with less cardiovascular risk.
The Lifetime Achievement Award was given this year to Maria Blasco, a veteran geroscientist whose contribution to the longevity field is formidable. After a short ceremony Maria proceeded to give a keynote talk on telomeres, the leading topic of her research for the last three decades. Maria described some of the most important experiments with telomeres. For instance, telomerase deficiency in mice causes accelerated aging, while transgenic mice with extra-long telomeres live longer and, importantly, get less cancer, which is the leading cause of death in lab mice. These mice also showed significant improvements in healthspan: better metabolism, less cognitive decline, less osteoporosis, and so on. Another study that Maria mentioned might provide an explanation of why turning back telomerase expression seems to lower the risk of cancer instead of elevating it: shorter telomeres cause chromosomal instability, which increases the risk of oncogenic mutations. Genetically engineered telomerase-expressing mice were more protected from cancer even when challenged with oncogenic mutations.
Melissa King has over two decades of experience in business, non-profits, and public affairs. About two years ago, she co-founded Healthspan Action Coalition with another veteran medical research advocate, Bernard Siegel. Melissa has steered important campaigns and projects in patient advocacy and biomedical research funding. For example, she led a successful ballot initiative in California to secure $8.5 billion in funding for the California Institute for Regenerative Medicine, which specializes in stem cell research. Patient advocacy, Melissa argued, is impressively effective in mobilizing public opinion and funds for health research initiatives. Now is the time to apply the principles of patient advocacy to prolonging healthspan. After all, when it comes to aging, every person on the planet is a patient. This creates a potential for a truly massive movement.