A brain passionate about science can do wonders for the world. While many young people diligently ace their science exams, few have a larger-than-life goal. They wonder, ‘What should I do with all this knowledge?’ Well, for Giriraj Ratan Chandak, former chief scientist and Sir JC Bose Fellow at the CSIR-Centre for Cellular and Molecular Biology (CSIR-CCMB), the answer was always within: a passion that lies in combining genetics with patient care and translating that knowledge into public health impact. “I have always felt a deep responsibility to give back to society in whatever way I could,” expresses Giriraj, who steers a startup called Lightening Lives LLP. In an insightful interview with CE, he speaks about his journey, startup, and more.
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Tell us about your startup: what does it do, and what kind of impact are you hoping to make?
I have had a deeply satisfying career at the Centre for Cellular and Molecular Biology. Yet, for a physician and scientist, the journey never truly ends. I realised there were many unfinished goals I still wished to pursue. To carry that vision forward, I founded a startup called Lightening Lives LLP.
As the name suggests, the ethos is to ‘light a lamp’ in people’s lives — whether by addressing genetic disorders, improving health, enabling treatments, or bringing hope in any possible way. Through this startup, our objective is to develop very simple, rapid, and affordable tests that can reach the most underserved sections of society. My years of work in genetic testing have confirmed that we are still only scratching the surface; with traditional approaches, barely 3–5% of patients undergo testing. The situation has only become more pressing with the rise of large-scale, high-throughput genetic testing, which often remains inaccessible to those who need it most.
At Lightening Lives LLP, we decided to focus on ‘commonly occurring rare diseases’ such as thalassaemia, sickle cell anaemia, and muscular dystrophy, using simple, robust protocols. I am proud to say that along with CSIR-CCMB, we have developed a test for sickle cell anaemia that requires just a drop of blood and costs less than ₹100, making it possible to bring accurate diagnosis directly to the communities that need it most. We are on the path for doing the same for beta thalassemia.
We have already expanded our work to include many other genetic disorders, with a clear focus on working at the grassroots level through the public health system. This means engaging directly with primary health centres, empowering ASHA workers and other community health personnel to identify patients, collect samples, and ensure timely diagnosis. In parallel, we aim to strengthen infrastructure at the hospital level so that these tests can be performed locally and treatment can be initiated without delay. This model has already shown success in several districts, and we intend to replicate it across different parts of the country.
You’ve spent decades working at the intersection of genetics and public health. Could you take us back to the beginning — what first sparked your interest in science, and later, in genetics?
I am a physician by training and a scientist by curiosity! My interest in genetics began as a curiosity — first sparked during my surgery training in paediatric cases such as cleft lip, cleft palate, and neural tube defects, where surgery was often the only option. I found myself wondering why these conditions occurred at all and whether they could be prevented in the first place. That curiosity deepened through a more personal observation: a colleague from Bengal who looked strikingly similar to me despite our vastly different backgrounds. It fascinated me that two people from such distant parts of the country could resemble each other so closely, yet be so different in personality and culture.
Over time, my training led me to focus on monogenic genetic disorders like thalassaemia and sickle cell anaemia. Here, we could identify disease-causing mutations, detect carriers, and work towards prevention of the birth of an affected child through prenatal diagnosis and genetic counselling. This became my true passion. For the past 25 years at CCMB, I have worked to translate this passion into action, establishing one of the first molecular diagnostics laboratories in a public setup. Our focus has been on developing simple, robust, and affordable genetic tests that could reach patients at a nominal cost, making prevention and care accessible to all.
You’ve done pioneering work in understanding genetic predispositions to complex diseases in Indian populations. What are some key differences you’ve observed between Indian and Western genetic patterns in relation to lifestyle diseases like diabetes or heart disease?
While rare genetic disorders like thalassaemia, sickle cell anaemia, muscular dystrophies, etc., seemed at first to have a straightforward genetic basis, we soon discovered that many of these diseases, though caused by the same mutation, did not present with the same clinical picture. What initially appeared to be ‘simple’ disorders began to reveal their complexity. A single genetic change could lead to very different disease courses, responses to treatment, and overall outcomes. We noticed similar patterns when studying non-communicable diseases such as type 2 diabetes, chronic pancreatitis, and cardiovascular disorders, where the genetic contribution was clear but the clinical expression varied widely.
Being a physician, I naturally developed a knack for noticing phenotypic and clinical differences between Indian and Western patients. Later, as a trained geneticist, this observation evolved into a deeper question: why do certain diseases manifest differently in Indians? Is our genetic architecture distinct from that of Western populations? Moreover, for many conditions such as diabetes and heart disease, I knew lifestyle and environmental factors played a major role alongside genetics. This made it essential for me to understand the genetic basis of diabetes in Indians, how it differs from Western counterparts, and how factors like nutrition, lifestyle, and environment contribute to disease risk. While we cannot change a person’s genetic makeup, we can modify lifestyle — and if we understand the interplay between genes and environment, we can create highly targeted strategies to prevent disease at the population level.
It truly felt like a magical journey at first; we kept discovering distinct mutations, whether in chronic pancreatitis, diabetes, or neural tube defects. Whatever diseases we examined, there seemed to be unique differences in genetic susceptibility among Indians. But the magic and suspense did not last long. We soon realised that genetics explained only a small part of the overall risk. The common thread lay elsewhere — in differences in lifestyle. I often remind audiences that changing the genetic makeup of a population takes generations, whereas environmental factors such as diet, stress, and nutrition can shift dramatically within just one generation, as we are seeing now with millennials and Gen Z.
And lo and behold, we began uncovering fascinating differences in the genetics of common traits such as obesity and height. As you know, obesity is a major risk factor for the future development of cardiometabolic syndrome. So, it was particularly exciting to find genetic variations that could clearly predict the ‘Indian’ pattern of obesity — more central and visceral — compared to the ‘European’ type of obesity.
There’s a lot of buzz around genome editing today. Some people imagine it as a way for parents to ‘design’ their children. What’s your take on that — is it hype, hope, or cause for concern?
The ultimate goal of any genetics research — beyond understanding the basic mechanisms — is to find ways to influence the clinical course of a disease, which is what we call management. But the definitive treatment for a genetic disease would be to correct the underlying mutation, restoring it to normal. This is the principle behind genome editing: the ability to fix the ‘mistakes’ in our DNA and bring the genome back to its intended state. It sounds simple, almost magical, but in reality, it is far easier said than done. While research in this area has been ongoing for two to three decades, it is only now that we are beginning to see the first truly beneficial effects emerge.
The most successful genome-editing stories so far have come from diseases like sickle cell anaemia, where the change required is just a single base correction. In contrast, the concept of ‘designer babies’ — where parents choose traits for their children — is largely hype, and in my view, a cause for concern. Such practices could disrupt the natural equilibrium of society, and I believe they should not be permitted without stringent regulations. That said, there is a narrow, ethically defensible scenario: when a couple chooses to have a genetically matched child so that tissues, particularly from the umbilical cord, can be used to treat an older, affected sibling. In such cases, the umbilical cord stem cells may offer life-saving therapeutic potential.
India faces a dual burden of malnutrition and obesity. How can genetic research help us understand and address this paradox?
India is a fascinating country in many ways: it has passed through distinct stages of malnutrition, followed by phases of overnutrition. This imbalance, moving from undernutrition in early life to overnutrition later, has contributed to a unique pattern of obesity known as central obesity. It is characterised by thin arms and legs but excess fat around the abdomen, a body type often referred to as the ‘thin–fat Indian’. This phenomenon has been debated widely, with some researchers proposing the ‘thrifty’ or ‘survival’ hypothesis — the idea that certain traits evolved to store energy efficiently during times of scarcity — while others point to specific genetic variants selected to protect against diseases like diabetes or metabolic syndrome. Whatever the cause, it remains a critical public health challenge because it serves as a major risk factor for cardiometabolic diseases.
This central obesity pattern acts as a forerunner for a wide range of non-communicable diseases, including metabolic syndrome, breast cancer, and many others. Therefore, it is crucial to understand not only its genetic basis, but also the lifestyle and nutritional factors that contribute to it. Equally important is exploring how nutrition and lifestyle can influence genetic susceptibility — an area of research that has given rise to the fascinating field of epigenetics.
Epigenetics is one of the most exciting frontiers in biology today. Can you explain what epigenetics is to our readers, and also, do you see this field transforming healthcare, especially in a country like India?
Epigenetics is indeed the exciting ‘new baby’ on the horizon. This field has emerged from the realisation that identifying genetic variants alone cannot fully explain the risk of non-communicable diseases. It is now understood that the genetic risk an individual is born with can be modified — for better or worse — by factors such as nutrition, lifestyle, and stress responses. In Indians, this modulation appears to play an especially significant role. In our own studies, we have found that genetic variants which strongly predict disease risk in Europeans often do not have the same predictive power in Indian populations.
In Indians, environmental influences often regulate the activity of these genes. We have shown that the effect of genetic predictors for traits like obesity and height in Indians is actually lower than in Europeans. However, when we factor in components of epigenetic regulation, their impact becomes much greater. This is both exciting and encouraging, because while genetic risk is fixed, environmental and lifestyle factors, which can be modified, have the power to significantly influence that risk.
This naturally leads to an interesting and important area of research known as the Developmental Origins of Health and Disease (DOHaD), a field I have worked in for the past two to three decades. The central hypothesis is that early-life factors influencing the clinical phenotype of the foetus act as a forerunner for the future development of cardiometabolic problems. In essence, maternal nutrition — through epigenetic regulation of risk genes — can affect the likelihood of conditions such as type 2 diabetes or cardiovascular disease in the child. The encouraging part is that if we can identify these factors, we can intervene, either by modifying them or by providing targeted supplementation, to reduce future risk. One such factor we have studied extensively is the micronutrient vitamin B12.