An Interview with Eric Verdin of the Buck Institute for Research on Aging

Eric Verdin is the present CEO of the Buck Institute for Research on Aging. From my perspective most of the research programs carried out there, with the notable exception of matters involving cellular senescence, is fairly distant from the SENS rejuvenation research we’d like to see prosper. The Buck Institute as a whole reflects the broader research community focus on greater understanding of how aging progresses at the detail level, absent intervention, and on the development of ways to modestly slow the accumulation of damage, such as calorie restriction mimetic drugs.

Thus even among those researchers interested in treating aging as a medical condition, our community still needs to persuade many more of them to work on damage repair strategies capable in principle of producing rejuvenation in the old, rather than tinkering with metabolism to merely slow down the rate at which damage accrues. The hope is that as SENS approaches such as senescent cell clearance show themselves to be far more reliable, as well as cheaper and faster to bring to the clinic, this will happen. Meanwhile we have the existence of numerous research centers of a size comparable to the Buck Institute, with ten times the annual budget of the SENS Research Foundation, working on comparatively little that can possible produce meaningful outcomes in aging in the near future.

Biologist Eric Verdin considers aging a disease. His research group famously discovered several enzymes, including sirtuins, that play an important role in how our mitochondria – the powerhouses of our cells – age. His studies in mice have shown that the stress caused by calorie restriction activates sirtuins, increasing mitochondrial activity and slowing aging. In other words, in the lab, calorie restriction in mice allows them to live longer. His work has inspired many mitochondrial hacks – diets, supplements, and episodic fasting plans – but there is not yet evidence that these findings translate to humans.

Why is there so much energy and excitement surrounding aging research right now?

Something happened in the 1990s. There were three groups that did an experiment that was really unexplained. Those groups all identified unique mutations in laboratory species that could actually increase lifespan. At that time, it was a quite astute observation in the way they completely turned upside down our conception of what aging was. The whole idea of aging was sort of an entropy problem where everything falls apart like your car rusting, but what these papers showed is that you can make a single change in one whole organism like C. elegans with a 100 million base pair genome, and you can double its lifespan. That by itself was mindboggling for a lot of people and suggested there might be pathways to regulate aging, and if there are pathways that means there are proteins, and that means you can eventually develop drugs. Today we’re at a point where people are considering starting clinical trials. This is why there is so much excitement and interest.

The Buck Institute focuses on research aimed at increasing healthspan. What do you mean by healthspan?

The whole mission of the Buck is not only to increase healthspan but also lifespan, but we don’t want to increase lifespan at the expense of healthspan. Every decade over the last hundred years, lifespan has increased by two years. That’s amazing because we’ve gone from an average life expectancy in the 1900s, which was around 47, to 77 today. That’s an incredible achievement, but this extended lifespan is not all rosy. We also have an epidemic of what we call the chronic disease of aging.

Can those incredible increases in lifespan continue? Is there an upper limit?

There currently is an upper limit, and the upper limit is probably around 115, 120. You have a very large number – 100 billion people to choose the number of people that have ever lived – and you have only one who has made it through to 122, Jeanne Calment. The second oldest was 119. That’s already a pretty good limit. If we could all live to 110 healthy and a disease in the last five years of life, I think most people would sign for this. But this does not anticipate future developments in biology. I’ve been in experimental biology for about 30 years. What we’re doing today is just amazing in comparison to what we were doing when I started. You can’t imagine what we will be able to do in biology in 30, 50, 100 years. That’s why I don’t like the idea that there’s an absolute upper limit that man will never live above 120.

Why isn’t there more interest in aging research in the larger biomedical community?

Aging research is a real paradigm shift in a way that really changes much of what we think about these chronic diseases. I think the biggest resistance is from medicine because medicine is organized in a way that is not so compatible with what we’re doing. Medicine is organized based on organs. You have a heart attack, you go see a cardiologist, and he’s going to take care of your heart by deferring the risk for heart attacks and controlling high blood pressure or high cholesterol. What our field is proposing is that aging is the major risk factor for all of these diseases. We should start targeting not cholesterol and blood pressure. I mean, you still have to do this, but if you start targeting the mechanism of aging, you will have a much more profound effect against all of these diseases. That really is the promise of what we’re doing.




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