Cynthia Kenyon Quotes

Well, we can study aging in people, but of course those studies take decades. So what we try to do is we use simpler organisms to try and understand the basic mechanisms and so in my laboratory, for example, we use things like simple baker's yeast that we use to make bread.

In the early '90s, we discovered mutations that could double the normal life span of worms.

The old age of lower mammals presents characters similar to those found in man.

You can open up a centenarian's brain, and you'll see some areas that look like that of a 50-year-old or of a 110-year-old. You can have variation in the basic process of aging, called senescence, in different parts of the same body.

I don't see any absolute biological limit on human age.

Imagine that: If you could change one of the genes in an experiment, an aging gene, maybe you could slow down aging and extend lifespan.

Anti-aging is an extremely under-explored field.

I thought that tackling aging and the mechanisms that promote life would be worth figuring out. I wanted to learn why it is that some people are healthier than others and why some people live to 110 and others only to 60 or 70.

We are slowly isolating the genes involved with the aging process. We do not have the fountain of youth, but I think, in the coming decades, we will unravel the aging process at the genetic level.

I am confident that when I get really old, the human lifespan will be extended.

Aging is mostly the failure to repair.

It's possible that we could change a human gene and double our life span. I don't know if that's true, but we can't rule that out.

It's a tender and complicated dance, watching our parents age. We become protective in ways we never were before, and we study them with a mix of sadness and curiosity: Is this what we will be like when we are their age? We tell ourselves to be patient - just answer the same question again as if it wasn't answered a moment ago.

Lifespan extension has never really been a goal of aging science, nor should it.

Aging is not one process. It's many different things going on that cause us to age. I have a program that at least slows down each of these different processes.

In humans, the thing is that as we mature, our telomeres slowly wear down. So the question has always been: 'Did that matter?' Well, more and more, it seems like it matters.

It is, of course, quite natural that a biologist whose attention had been aroused by noticing in his own case the phenomena of precocious old age should turn to study the causes of it.

We know in the field of aging that some people tend to senesce, or grow older, more rapidly than others, and some more slowly.

I'm the chief science officer of a foundation that works on the application of regenerative medicine to the problem of aging.

Telomeres are the ends of our chromosomes that control how long we live. As telomeres become shorter, then cells age and die more quickly. In simple terms, as your telomeres get shorter, your life gets shorter.

We know that people who are born with shorter telomeres than normal also have a shorter lifespan. We know that shorter telomeres can cause a shorter lifespan.

Only 20 percent of our longevity is genetically determined. The rest is what we do, how we live our lives and increasingly the molecules that we take. It's not the loss of our DNA that causes aging, it's the problems in reading the information, the epigenetic noise.

The way to make a worm live longer is probably quite different from making a human live longer.

Science is telling us that the reason people die is not because some god said so or because the laws of nature mandate it. People always die because of technical problems. And every technical problem has, in principle, a technical solution.

When I started in the field, aging research was the backwater of biology. The idea that you could find a molecule that would prevent many diseases at once was considered impossible.