The Dutch Famine, a severe period of starvation in the German-occupied western Netherlands, occurred during the final months of World War II (late 1944 to early 1945). Also known as the “Hongerwinter,” this event affected approximately 4.5 million people in a previously well-nourished population. The precise and well-documented nature of this famine, with clear onset and relief, transformed it into a unique “natural experiment” for scientific inquiry. This context provided an opportunity to study the long-term biological effects of nutritional deprivation on human health across generations.
The Famine’s Genesis
By late 1944, Allied forces had liberated parts of southern Netherlands, but the western regions, including major cities like Amsterdam, Rotterdam, and The Hague, remained under German occupation. In September 1944, the Dutch government-in-exile called for a national railway strike to support the Allied advance. The German occupiers retaliated by imposing a severe transportation embargo, cutting off food and fuel supplies to the western Netherlands.
This blockade coincided with one of the harshest winters in recent memory, compounding the crisis. Freezing temperatures rendered waterways impassable, preventing alternative food transport and exacerbating the scarcity. The daily caloric intake for the affected population plummeted dramatically, averaging between 400 to 800 calories per day. People resorted to consuming grass and tulip bulbs to survive, highlighting the extreme nature of the caloric restriction during this relatively short but intense period of deprivation.
Immediate Physiological Toll
The severe caloric and nutritional deprivation during the Dutch Famine inflicted an immediate physiological toll on the population. Widespread malnutrition became rampant, causing significant weight loss across all age groups. The limited food availability led to a drastic reduction in the body’s energy reserves.
This acute starvation increased susceptibility to various diseases. Mortality rates surged, particularly among vulnerable groups. Between 18,000 and 22,000 people died during the “Hunger Winter,” with older men being disproportionately affected. Babies born during this period were smaller, reflecting the direct impact of maternal undernutrition on fetal growth and development.
Intergenerational Biological Consequences
The Dutch Famine Birth Cohort Study, tracking individuals born around this time, has revealed intergenerational biological consequences. Those exposed in utero faced increased risks for a range of metabolic disorders in adulthood, including type 2 diabetes and obesity.
Cardiovascular health was also impacted, with findings indicating a higher prevalence of coronary heart disease, a more atherogenic lipid profile, disturbed blood coagulation, and elevated stress responsiveness among those exposed in early gestation. Psychiatric conditions also showed increased risks, such as schizophrenia, anxiety, depression, and antisocial personality disorders. The concept of the “developmental origins of health and disease” (DOHaD) emerged from such observations, proposing that environmental factors during early development can “program” an individual’s long-term health trajectory.
A proposed mechanism for these lasting effects is epigenetics, involving changes in gene expression without altering the underlying DNA sequence. Studies found that individuals exposed prenatally to the famine, particularly during the periconceptional period, exhibited persistent differences in DNA methylation, specifically at the imprinted IGF2 gene, even decades later. Alterations in methylation were also observed in other genes involved in growth and metabolism, including IL10, INSIGF, LEP, MEG3, ABCA1, and GNASAS. This epigenetic mechanism suggests how early environmental cues, like nutritional deprivation, can leave a lasting biological legacy.
Advancing Human Biology Through Famine Research
Research stemming from the Dutch Famine has advanced our understanding of human biology, especially regarding the long-term impact of early-life nutrition on adult health. The famine’s precise timing and severity, combined with historical records, allowed scientists to identify specific “critical windows” of development. This research demonstrated that the stage of gestation during which undernutrition occurred influenced the type and severity of adult health outcomes, with early gestation often appearing as a particularly vulnerable period.
The famine studies provided human evidence for the DOHaD hypothesis, illustrating how poor maternal nutrition during pregnancy can lead to permanent structural or functional changes in organs and tissues, predisposing individuals to chronic diseases later in life. These studies also provided support for the role of epigenetics in mediating these long-term effects, showing how environmental conditions can induce lasting changes in gene regulation. This body of work has implications for public health, emphasizing the importance of adequate maternal nutrition and early-life conditions for preventing chronic diseases across generations. These insights underscore the interconnectedness of early environmental exposures and lifelong well-being, informing preventative medicine and nutritional science globally.