One of the most popular sessions at the 2026 South Asian Literature and Art (SALA) Festival featured Nobel Laureate Dr. Venki Ramakrishnan in a discussion on “The Science of Death.” The event, moderated by science journalist Angela Saini, was held at Menlo College, Atherton, CA, on Sept 26th.
Ramakrishnan’s book, Why We Die: The New Science of Aging and the Quest for Immortality, brings together biology, history, and ethics, blending scientific rigor and accessibility for a general audience. Kirkus Reviews called it “an illuminating account of the science of life extension with a more critical eye than most.”
In an exclusive interview with Raji Pillai for India Currents, Dr. Ramakrishnan discussed his journey, the next frontiers in science, and what lies ahead. This interview has been edited for brevity and clarity.
Raji Pillai: You studied physics in college in Baroda, and then went on to obtain a PhD in Physics. Tell us about your move.
Dr. Venki Ramakrishnan: I was not actually a very good physicist. I left physics because I didn’t think I would do very well in it as a career. 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. You can think of me as a failed physicist.
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.
RP: How did you find 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 Laboratory, 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 the 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.”
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 about the structure of the ribosome. So much has happened in terms of applications for DNA structure. Similarly, for ribosome structure, what do you see as potential applications?
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 the 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.
RP: You said 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.
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?
VR: 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.
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.
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.
Raji Pillai lives in the SF Bay Area and writes at www.rajiwrites.com. This article was informed by her training and profession as a scientist.
