Everyone complains about aging, but nobody seems to do anything about it. At least, not at its core. For every anti-aging wrinkle cream and memory enhancement product that promises to stave off the inexorable toll that time exacts on human bodies, there are precious few resources allocated to studying the fundamental processes that are actually making usand all other living thingsage.
"There is a lot of interest in interventions in the black box of aging, but much less in shedding some light into that black box."
Unlike say, L'Oreal, Dr. Jan Vijg, chair of the genetics department at the Albert Einstein College of Medicine, is actually looking into it. Working with the SENS Foundation, whose aim is to "advance rejuvenation biotechnologies," Vijg examines individual neurons in mice in order to determine what factors are causing them to age. While much of the aging process remains a mystery, it's clear that it emerges as a result of nature's preference for the young. "Life on earth is a matter of reproduction, not indefinite preservation," Vijg says. "This is why genes are molded during evolution to provide benefits at earlier ages, i.e., to reach reproductive age in an optimal way."
In the following interview, which was conducted over email and edited for clarity, Vijg tells Gelf why medical technology research may have plateaued, what circumstances lead genes to promote longevity, and why morality doesn't even in play into the age equation.
Gelf Magazine: How is the conversation about aging changing?
Jan Vijg: My sense is that over the last decade the focus has moved more towards interventions. People see that it is actually possible to intervene in a myriad of ways to extend life span and health span in animal models, from worms to mice and monkeys. This comes a little bit at the cost of gaining a better understanding of what aging is all about. We still don't know the causes of aging, to a large extent due to the difficulties in getting descriptive research funded. There is a lot of interest in interventions in the black box of aging, but much less in shedding some light into that black box.
Gelf Magazine: What about the aging process remains mysterious to us?
Jan Vijg: Basically everything. There is virtual consensus about why we age (after reproduction the force of natural selection declines, thereby not getting rid of genes with late adverse effects), and also about the basic causes (damage accumulation). However, opinions differ about the types of damage that are important and the mechanisms through which damage exerts its effects and causes functional decline, structural deterioration and increased disease.
Gelf Magazine: Specifically, what is the role of genetics in aging and mortality?
Jan Vijg: Your genes are primarily interested in your life cycle, not in preserving you indefinitely. Short-lived organisms are as successful (some would say much more successful) than long-lived organisms. Life on earth is a matter of reproduction, not indefinite preservation. This is why genes are molded during evolution to provide benefits at earlier ages, i.e., to reach reproductive age in an optimal way. However, they can sometimes be shaped to promote longevity as well. In a benign environment without predators, individuals at older ages can also reproduce and this will gradually lead to an increase in life span. In general, genetic variation within a species controls life span, but not usually deliberately. For example, gene variants that make you grow fast and furious are at an advantage in the wild because you dominate your environment and can enjoy lots of reproduction. At older ages, however, (which you will rarely if ever enjoy because of your aggressive lifestyle) your pro-growth signaling pathways run amok in your cells, causing cancer and rapid deterioration. On the other hand, those timid individuals without those gene variants that would probably rarely reach reproductive age in the wild will do so in a regulated, protective society. Later in life, their slow growth signaling pathways will help them to protect their biomolecules better, so they can live longer. There is evidence for an antagonism between growth and reproduction on the one hand and somatic maintenance on the other.
Gelf Magazine: What is the goal of the SENS Foundation? What is it you do with them?
Jan Vijg: My research focuses on the possibility that aging is caused by genomic and epigenomic drift, i.e., that the gradual accumulation of random mutations and epimutations (which are irreversible) will reduce the accuracy with which our cells signal messages and carry out specific functions. If this is true then there is very little you can do about that. SENS assumes that aging is caused by damage, but not that kind of damage. They assume aging is caused by chemical damage, which we can fight using enzymes to cut open protein aggregates, antibodies to help getting rid of senescent cells, etc. But how can you fight DNA errors that are irreversibly accumulating in all your cells and are different from cell to cell? They asked me to test directly if this could be true for the mouse brain, by looking into a number of individual neurons to see if we can find evidence for epigenomic and genomic drift. I describe the genomic/epigenomic drift hypothesis in my book Aging of the Genome: The Dual Role of DNA in Life and Death.
Gelf Magazine: In your view, can medical professionals expect to make dramatic progress in intervening in the aging process?
Jan Vijg: In my latest book that just came out The American Technological Challenge: Stagnation and Decline in the 21st Century, there is a chapter on medical technology in which I briefly address the issue of whether or not we can expect further dramatic progress in medical intervention, including interventions in aging. The answer is no, and the reasons are very similar to why we still fly in the same planes as 60 years ago, never went to Mars, there are still garbage men in New York to pick up your trash from the streets and why in winter we still have to accept heaps of snow on our streets and closed airports.
Gelf Magazine: Might there be other methods of extending life that don't have to do with reversing genomic drift?
Jan Vijg: Yes, for example, Aubrey de Grey does not believe that genomic or epigenomic drift are major causes of aging. He believes there is chemical damage such as protein aggregates. Others believe it's mainly a matter of increased inflammation (inflammaging). And there are still a tiny few who continue to believe that aging is programmed. Overall, genomic or epigenomic drift is just something that most people would consider as a possible contributor to aging. I happen to work on it, but don't think that this is the only game in town.
Gelf Magazine: Though it may be biologically factual, it's still striking to hear you say, "Life on earth is a matter of reproduction, not indefinite preservation." Is there a moral element that comes into play when dealing with matters of aging?
Jan Vijg: Not for me. I have no qualms whatsoever to strike out against nature's principles.