Antibiotics work by killing bacteria, stopping infections from running rampant. Antivirals work by killing viral replication. Cancer drugs kill (hopefully) tumors. Anti-depressants effectively shut down certain pathways associated with depression.

The fact is, most drugs we use today are killers — or to put it another way, inhibitors of some process we want to stop — rather than a way to engender some process we do want.

This all makes sense, when you consider the fact that biology as a whole is still pretty poorly understood. Imagine transporting a modern car back to 1700, into the hands of our greatest scientists of that era, and asking them to fix a transmission, or maybe design a new and better one. It’s hard to imagine they could fix anything, let alone improve on it; they would very likely damage the car in an attempt to fix the problem.

This, effectively, is the era we are still in in biology — trying to solve problems we don’t yet even fully understand.

There’s also the fact that modern healthcare is generally poised to handle specific indications — i.e., to treat some specific disease and problem, rather than improve general health. Modern diagnostics (Dx) and therapeutics (Rx) all currently exist within a framework for treating disease, and one’s indication guides treatment. This derives from both regulatory policy as well as reimbursements. Within a given indication, so much biomedical research follows in these footsteps of Dx and Rx.

But we’re beginning to see a groundswell in a new direction for both biology and health: away from killing, stopping, halting, shutting down… and towards healing, or prevention. In other words: towards promoting health. It’s starting to look like Dx and Rx are only two small pieces of a much larger solution, where prevention — let’s call it “Px” — explicitly becomes part of the medical arsenal.

This all starts with a tale of two mice. In 2014, Tony Wyss-Coray and his co-workers published their work on parabiosis of young mice with old, literally connecting the blood of young mice into old and vice versa. This work follows on the shoulders of many giants, including Tom Rando’s lab’s work from 2005 on rejuvenation of cells given a young systemic environment. The results were astounding: Something in the blood of young mice restored youthful cognitive function in old mice, essentially healing the old mice.

While this has been picked up in popular culture as a kind of Dracula-like story about the possibilities of eternal youth, its significance is in fact much more concrete. It indicates that some causative therapeutic agent (still unknown, but carried in blood) could possibly address not just one, or two, or three specific diseases, but the wholesale degradation that happens to our body with age. Suddenly, it’s possibly to think of age itself as an indication. Once again this shifts away from halting or stopping aging — we won’t, and can’t, live forever — to preventing degradation.

What happens when you focus not on stopping aging, but on increasing the length of time when you are at your healthiest?

Since then, there has been a flurry of activity to identify the elements in youthful blood either as a diagnostic and/or potentially as a therapeutic. One of the core challenges in doing so is this: How can one even identify a drug as being successful for combating aging? At first glance, you would think it would require decades in testing, with very slow cycles for innovation. How else to measure living longer but for years to pass?

Identifying key biomarkers can speed this process up enormously. An analogy to a better-understood area — heart disease — can illuminate how: We know that Atorvastatin (sold as Lipitor) works to impact heart disease in a patient not by waiting for decades to see if the patient develops heart disease, but because there is a well-known biomarker that correlates with cardiovascular disease: cholesterol. With the knowledge of that relevant biomarker (cholesterol is tightly linked to heart disease), cholesterol becomes a powerful tool for drug development and patient treatment.

Could the equivalent biomarker be discovered for aging? Given the parabiosis results, the answer is likely waiting to be discovered in youthful blood. I’m thrilled to announce our investment in BioAge, a startup that’s taken on this combined biochemical and data science challenge to identify these agents. The potential implications are huge: from testing existing treatments for longevity (that have been posited to date) as well as for developing enhanced new drugs (that engender the desired properties). BioAge’s team has unique expertise in this area, bringing together CEO co-founder Kristen Fortney’s expertise in ageing, biochemistry, and bioinformatics with a fantastic team of biochemists and data scientists. BioAge is architected, team-wise, to develop tools that enable them to rapidly identify these causal agents.

The implications of success here are mind boggling, perhaps even extending the average lives we expect to lead. And what we really mean by “life extension” would likely mean stretching one’s healthy years, living healthier longer, perhaps in addition to adding years to the end of our lives. It brings us closer than we think to a world where “120 becomes the new 80” and 60 is literally the new 40. BioAge’s results to date in assaying the molecular nature of youthfulness lays the first brick in the road towards this future.




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