What Barker proposed was that heart disease, diabetes, and stroke do not begin in adulthood but in the womb, and not merely from genes but also a foetus’s biological response to its mother’s diet. Photograph used for representational purposes only
| Photo Credit: Getty Images/iStockphoto
It was a routine morning at a government primary health centre in an agricultural belt, when a 68-year-old man arrived for a follow-up consultation. A retired farmer, he led a quieter life—helped by his children, spending his days at home. Yet his blood sugar levels remained persistently high. Sitting beside him was his son, a software engineer, who remarked, “Appa worked in the fields for over 40 years. He never sat idle. How come someone so physically active ends up with diabetes now?” As a doctor, I found myself pausing—not for lack of an answer, but because the question touched a deeper nerve. It challenged our conventional wisdom, especially when the patient’s lifestyle seemed protective on paper. The explanation however, lay not in what the father had done in his adult life but in what he was exposed to long before he took his first breath. This is the crux of the Barker Hypothesis, or the Foetal Origins of Adult Disease. This idea invites us to look inward and backwards into biology in the womb.
Barker’s bold hypothesis
David Barker, working with historical data from England, noticed that regions with higher infant mortality rates in the 1920s, subsequently had more deaths from heart disease in the 1970s. He connected the dots: poor foetal nutrition programmes the body for thrift. A foetus that “learns” it is growing in a starved environment slows down metabolism, alters organ development, and conserves fat. But when it is later exposed to calorie-rich food, these programmed adaptations backfire—leading to conditions like type 2 diabetes and hypertension. What Barker proposed was that heart disease, diabetes, and stroke do not begin in adulthood but in the womb. And not merely from genes but also a foetus’s biological response to its mother’s diet.
When exposed to undernourished or adverse conditions in the womb, which typically happens in undernourished mothers or during famines, the foetus begins to remodel itself by altering the structure and function of vital organs to preserve brain development and improve its chances of survival. This developmental compromise prioritises the nervous system, often at the expense of other organs — the kidneys, pancreas, and liver. Such adaptations are designed to prepare the foetus for a life of continued scarcity after birth—a concept known as plasticity, which is an evolutionary advantage in unpredictable environments. However, this advantage becomes a liability when the external environment after birth turns out to be one of plenty. As a result, the mismatch between prenatal expectations and postnatal realities becomes a fertile ground for non-communicable diseases. The child, now equipped with a metabolism tuned for famine, faces a world of caloric abundance. The same physiological adjustments that once ensured survival can now predispose the individual to chronic illnesses including diabetes and hypertension. This process is known as programming: when early life stimuli, particularly during foetal and early childhood stages, lock in long-lasting changes.
This hypothesis explains contrasting outcomes from the two most studied famines in history: the Dutch Hunger Winter (1944–45) and the Leningrad Siege (1941–44). In the Netherlands, starvation was intense but short-lived. Post-famine, the external environment rapidly normalised. Children exposed to famine in the womb suddenly found themselves in well-fed childhoods. This metabolic mismatch led to high rates of diabetes and obesity decades later. Leningrad, however, experienced prolonged starvation. Even after birth, the environment remained malnourished. There was no mismatch, and hence, fewer signs of metabolic syndrome. The lesson: it is not famine alone, but famine followed by a feast that does the damage. Despite numerous famines during colonial rule in India—the Bengal famine (1943), Madras famine (1876), Orissa (1866), and others—India lacks robust cohort studies linking them to modern diseases. Possible reasons include early deaths before chronic diseases manifest, the lack of diagnostic tools, birth registers, and the intent to study in the 20th century.
Lotteries and genes
I offer a metaphor. Imagine two families living in poverty. One family continues in deprivation, and while struggling, they learn to survive. The second family, also poor, suddenly stumbles upon a buried treasure or wins a lottery. At first, this seems like a blessing, but they soon spiral: they lose balance, relationships falter, indulgence grows, and stress mounts owing to lack of financial literacy. Their emotional and financial systems crash. This is akin to what happens when a foetus, programmed for scarcity, is suddenly exposed to affluence. It is a metabolic version of vertigo—as if the body has entered a roller- coaster it was never trained to handle. This is the essence of the Thrifty Phenotype Hypothesis, a refined version of James Neel’s Thrifty Gene Hypothesis, which argued that during prehistoric times—especially in the Palaeolithic and Neolithic ages in African savannas—humans evolved to store fat efficiently during food abundance to survive inevitable famines. Back then, it was an evolutionary advantage. Today, it is a metabolic trap.
A 2023 Scandinavian study of over 3.4 million births found that preterm and small-for-gestational-age (SGA) infants face higher risks of early cardiovascular disease. While sibling comparisons reduced the SGA risk —implying genetic factors—the preterm link remained strong, underscoring the role of intrauterine conditions. The World Health Organization (WHO) affirms that foetal undernutrition contributes significantly to chronic diseases like hypertension and diabetes. Prevention must begin not in middle age but with maternal care, prenatal nutrition, and safeguarding foetal health from the very start.
Caution against oversimplification
While evidence supports foetal programming, studies also caution against oversimplification. Birth weight, they argue, is a crude proxy. Preterm birth, small-for-gestational-age, and genetic-environmental interactions muddy the waters. While the Barker Hypothesis has its critics and caveats, its central message remains powerful: the womb remembers. The scars of deprivation, if not healed, can echo across decades.
In India, where millions are born into poverty and rise into a food/caloric-abundant society, the hypothesis is not just a scientific curiosity; it is from where an epidemic has emerged. A deeper investigation into Indian birth cohorts, perhaps beginning with those born before the years of the Green Revolution, may finally tell us whether Barker’s English findings have found their Indian twin.
(Dr. C. Aravinda is an academic and public health physician. The views expressed are personal. [email protected])
Published – May 12, 2025 06:00 pm IST