Nobelist Venki Ramakrishnan on living longer, his new book, and techie arrogance
Updated: 9 hours ago
Before the 2026 Nobel Prizes announcements rolled in, a 2009 laureate, Venki Ramakrishnan who shared the Nobel Prize in Chemistry (with Thomas Steitz and Ada Yonath) for elucidating the structure of ribosomes, spoke at the South Asian Literature and Art Festival (SALA) 2026, about his new book Why We Die, living longer and techie arrogance.
Dr. Venki Ramakrishnan informed and entertained a packed audience at the South Asian Literature and Art (SALA) 2026 Festival at Menlo College, Atherton, CA on Sept 26th, 2026 in a session entitled “The Science of Death”, moderated by science journalist Angela Saini. In a discussion about his book Why We Die (HarperCollins, 2024), Dr. Ramakrishnan switched from complex scientific topics which he explained in simple, occasionally humorous terms, to engaging rants about Silicon Valley tech billionaires and their desire to prolong life.
On Sept 27th, I spoke with Dr. Ramakrishnan about his journey, the next frontiers in science, and what lies ahead for him.
KEYNOTE SESSION HIGHLIGHTS
The Hubris of Techies
Within a 7-mile radius of this place, people want to live longer. They can’t buy youth, but they can buy aging research, and that is distorting the field. On scientists abandoning UCSF, UCLA, and the Salk Institute and going to Altos Labs, he understands the reason; getting funding for research is a slog.
He quoted amusing lines on the wealthy: “When they were young, they wanted to be rich. And now that they are rich, they want to be young.” He went on to slam people in tech who “see the brain as a computer. This is completely bonkers!” He went on to say “They are so arrogant with their successes in software that they see everything as a software problem. They don’t bother to learn biology. They see everything as a digital problem. Biology is analog, not digital.”
Research on Aging
Aging research has gained prominence in recent years as governments are "terrified" of a demographic cliff as fertility rates plummet, and want to know whether people can be kept healthy for longer. While life expectancy has risen from about 40 to 60 to 80 as child mortality, infectious disease, heart disease and some cancers have declined over the years, maximum lifespan is a separate question. He gave examples of long life: the Galápagos tortoise which may well have seen Darwin in the late 1800s, and Jeanne Calment, who lived to 122 with a daily cigar and glass of port after lunch (which he doesn’t necessarily recommend) and about 2½ lb of chocolate a week.
“Evolution doesn’t care how long you live,” he commented on the biological imperative: it cares about reproductive success. A mouse reproduces early, makes lots of offspring and is short-lived.
Anti-Aging Solutions
On proponents of anti-aging solutions, he exclaimed “some are nutty!” going on to talk about the business of freezing bodies to be revived years later. He asked the audience if they had ever frozen blueberries. Cryobiology is a science, but when people say they have frozen a mouse brain, they have just frozen a slice of a mouse brain. On cryonics, the practice of preserving a legally dead person at extremely low temperatures with the hope that future medical technology may revive and restore them, “When they freeze a mouse, unfreeze it and it runs around, I’ll take notice.”
Telling people their “biological age” is nonsense, he continued, as organs age at different rates.
“Bio-hacking”, data obsessions
On collecting enormous abouts of information people collect such as from rings: fitness rings or smart rings, he asked, what are you going to do with all the data? There’s little you can do, you’re just going to stress about it. “There’s nothing more stressful than a wedding ring,” moderator Angela Saini quipped.
He talked about the inequities of living longer: rich people live approximately 15 years longer than poor people.
On caloric restriction as a way to slow aging, Dr. Ramakrishnan named metformin and rapamycin which mimic caloric restriction, but studies are still under way to assess if they extend lifespan in people. Similarly, with GLP-1 agonists (“popular in California”), while longevity could be a potential benefit, GLP-1 affects many organs: e.g. causing muscle loss, just as aging does, and proper trials are needed to understand the true implications.
Why We Die: The New Science of Aging and the Quest for Immortality (William Morrow, 2024), which brings together biology, history, and ethics, has been praised as both scientifically rigorous and accessible to a general audience. Kirkus Reviews called it “an illuminating account of the science of life extension with a more critical eye than most."
INTERVIEW WITH DR. RAMAKRISHNAN
As a scientist, I was grateful for the opportunity to speak with one of the great minds in science at SALA 2026.
The Beauty of Physics, The Rewards of Biology
Raji Pillai: You studied physics in college in Baroda, and then went on to obtain a PhD in Physics. Tell us about your move from physics to biology.
Venki Ramakrishnan: I think I was not actually a very good physicist. No physicist would consider me a physicist. I left physics because I didn't think I would do very well in it as a career. And I became interested in biology. In fact, I went back to graduate school, to learn biology.
Physics is a beautiful, elegant subject. Exams weren't hard for me, but research was: thinking like a physicist, breaking problems down and making real progress. The abstraction and mathematics just keep increasing.
Biology is hard in a different way. It's a highly complex system, and you must design experiments that extract information from it. But it has had huge breakthroughs in the last 75 years, so the move has been rewarding.
Becoming a Biologist: UCSD and Yale to the National Labs and the LMB
RP: What was your journey into biology research in the US like, and how did you find your way your way to the UK, to the Medical Research Council Laboratory of Molecular Biology (LMB) in Cambridge?
VR: I went back to graduate school to learn biology. In my second year I wrote to Don Engelman at Yale, who had once offered me a postdoc I'd declined because I knew no biology: now I know some biology, and I even know what a ribosome is. He had no opening, but his collaborator Peter Moore, who worked on ribosomes, did. With very few publications and an odd career, for them to take a chance on me was remarkable. So I got into ribosomes almost by accident.
Ribosomes were out of fashion then. After completing my postdoctoral research, I sent out about 50 faculty applications and didn't get a single interview. Don arranged a job at Oak Ridge National Laboratory, which I soon realized was a dead end. Fifteen months later I moved to Brookhaven National Labs, where I really learned to be an independent scientist.
A turning point was a sabbatical from Brookhaven to the Medical Research Council (MRC) Laboratory of Molecular Biology (LMB) in Cambridge, the lab that pioneered so much, from DNA to the first protein structures. I learned crystallography there and realized it was actually possible to solve the structure of whole ribosome. The LMB had no job, so I went to the University of Utah, a beautiful place with great colleagues. But US grants run three to five years, and I sensed this problem might take far longer.
So I wrote to the LMB again. They liked my ideas but had no space, which I took as a polite no. Weeks later the director, Richard Henderson (2017 Nobel laureate in Chemistry), wrote that the space had materialized. It meant nearly halving my salary and my wife giving up her life in Utah. We went for a long walk and said, let's just do it. That was 27 years ago. I've now lived in Cambridge longer than anywhere.
Parallels between DNA and the Ribosome
RP: You went to a historic place, where the structure of DNA was discovered, by Watson and Crick in 1953, and years later, you made another historic discovery into the structure of the ribosome. Since the structure of DNA was discovered, and the human genome was sequenced, so much has happened in terms of applications of that knowledge. When you think about protein biosynthesis, and ribosomes, what do you see as the key things that have happened to push biology forward, either in the basic research sense, or towards an application?
VR: The ribosome is older than DNA. Without the need to make proteins, there'd be no need for DNA to store instructions for them. But DNA transformed biology by showing how information is stored and transmitted. The ribosome sits at the crossroads between genes and their products, converting information into proteins. It's far more complicated but hasn't captured the public imagination, partly because the double helix is simple and makes an instantly recognizable picture.
DNA's structure was solved in 1953, but making proteins from recombinant DNA came only in the '80s; then came PCR, and everything exploded. It took decades, and with the ribosome it may take longer. The obvious application is antibiotics, but goal of making antibiotics that are very specific to bacteria, but don’t affect humans, is a harder problem. Nature has done it many times, but enzymes humans lack entirely may be better targets. Penicillin is the classic case: bacteria have cell walls, and we don't. Further out, people are engineering ribosomes, and we might design new, precisely coded synthetic polymers. But I went into it for fundamental research reasons.
The (Digital) World According to Techies
RP: You mention in your discussion yesterday about how tech folks see all problems as digital. How do you see it?
VR: They believe everything in the analog world can be represented digitally, like pictures and sound. Maybe, but analog systems change dynamically. We don't understand the brain well enough to represent it digitally, and aging involves cells, tissues and the whole organism. I'm not sure they can just crank their computers and solve big problems. AI will be very powerful in chemistry, as AlphaFold shows, but may struggle with complex systems like biology. Then again, ten years ago I might have completely missed where AI is today.
The Next Frontiers, in Science, in Life
RP: What do you see as the next few frontiers in science, broadly, or in biology?
VR: The big questions are perennial: how does the brain work, how did life arise from chemicals, what is the origin of the genetic code, how did handedness (chirality) develop, and how does an egg develop into an organism? These are tough problems, especially the origin of life. Even how the ribosome evolved is fuzzy. Early ribosomes may have been RNA only. How did you go from little random peptides to something that actually is stored as a genetic code, and then you can make the same peptide over and over again? That's not at all clear. And so there are some big fundamental questions still left in biology.
RP: How long did it take you to write and publish your book? And now that you have closed your lab at the LMB, what lies ahead for you, in the next 5, 10, 20 years?
VR: In my book, I didn't mention GLP-1 drugs at all, because they were so recent. That is certainly an area where people are trying to do some work related to this whole class of caloric restriction drugs. They are not without side effects and a need for long term clinical trials.
Why We Die took three to four years: about a year of research, reading and interviews, two years of writing, and a year of editing.
I doubt that I will live 20 years. I'm already 74. But I don't really know. I just have to think about it. Many people make a long-term plan, and maybe I'm lazy mentally, or maybe I'm burned out. But I haven't really given much thought to what I want to do for the next five years or so.
The panel discussion report was published in India Currents on October 3, 2026.
My interview with Dr. Ramakrishnan was published in India Currents on October 8, 2026.
Comments