A Famine That Lasts Generations: Epigenetic Inheritance
Famine, the extreme scarcity of food, is a concept that has persisted over centuries: From climate change and poor harvests to strategic starvation as a weapon of war, starvation is no new phenomenon. Today, 266 million people are at risk of acute hunger and of that, 45 million are at risk of acute hunger because of ‘Middle East Conflicts’ (World Food Programme [WFP], 2026).
Gaza, Palestine, as of 2025, has been confirmed to be at IPC Phase 5 Famine (Integrated Food Security Phase Classification [IPC], 2026): levels associated with extreme malnutrition and mortality (quantified as two deaths out of 10,000 or four child deaths out of 10,000 per day). Similarly, Haiti experiences catastrophic IPC Phase 5 caused by violence and economic collapse; half of Sudan’s population is facing acute food insecurity or IPC Phase 3; around 7.7 million in South Sudan also face famine of IPC Phase 3+, and in Mali, approximately 1.5 million people face crisis levels of food insecurity or worse (Action Against Hunger, 2026). This is only a list of the regions experiencing the highest levels of starvation. Around 9 million deaths are caused by acute starvation, 25000 per day of which are > 10,000 children.
The reality is that the effects of famine last beyond the decades it strains a population. For those who survive, the evidence of starvation appears in the epigenome passed from parents to children. This essay explores how the biological residue of famine persists across generations, long after the hunger itself has ended.
Epigenetics is the inheritance of altered gene expression that is not caused by a change in DNA sequence (Peschansky & Wahlestedt, 2014). For an epigenome to be considered transgenerational (the epigenetic markers appear from one generation to the next), it must meet the criteria that the filial zero (the first generation) should be exposed to an event and the effect must be observed up to the third or fourth generation (Lacal & Ventura, 2018). The biomarkers of epigenetics include incorporation of non-canonical histone variants, chromatin remodelling, non-histone protein components, DNA methylation, DNA-binding proteins, RNAs and histone modifications (Winter & Fischle, 2010).
From 1944 to 1945, the Netherlands, then occupied by Germany, faced a winter known as the ‘Hunger Winter’, during which food rationing fell to as little as 500 kcal. The famine had major health effects on the population, even after it ended. A study by Heijmans et al. (2008) observed differences in IGF2 DMR methylation caused by periconceptional exposure to famine in Hunger Winter Families. The results showed that prenatally exposed individuals had significantly lower DNA methylation of the imprinted IGF2 gene six decades later, compared to their unexposed same-sex siblings. The IGF2 gene provides instructions for producing a peptide hormone that is critical for fetal growth, development, and cellular proliferation. Low methylation suggests reduced gene activity, and for the IGF2 gene, consequences include disrupted metabolism, impaired growth, and developmental syndromes.
Similarly, in the case of the Great Chinese Famine that lasted from 1959 to 1961, a study by Li et al. (2021) found a predominant pattern of decreased DNA methylation at four CpG sites caused by fetal exposure to famine. The sites are associated with genes EHMT1 — neurodevelopmental disorders (Kleefstra syndrome, autism), CNR1 — neurological phenotypes, Tourette syndrome, UBXN7 — expressed in the brain, function poorly understood, and ESM1 — previously linked to gestational diabetes exposure. Each altered expression is linked to dysregulated neurodevelopment, altered stress responses, and impaired metabolism, thereby increasing the risk for neuropsychiatric and metabolic diseases.
In the presented case studies, the individuals observed were children born or conceived at the time or near the time of famine. Of course, the inheritance of these markers would be the expected outcome. However, as noted before, for an epigenome to be considered transgenerational in mammals, it must persist to the F3 generation (the great-grandchildren of the exposed individual). Additionally, the epigenetic mark must be present on germline DNA (found in sperm or egg cells) and survive two major reprogramming events that normally erase most epigenetic marks after fertilisation. Although reprogramming typically wipes out or corrects most DNA methylation patterns, certain marks can persist and propagate across generations (Bender et al., 2025). This is especially true for DNA methylation, histone modifications, and small non-coding RNAs, which are the primary carriers of heritable epigenetic information. Hence, it can only be concluded that these epigenomes and their effects can trickle down for generations.
In conclusion, the grim reality is that an event can change the progression of life across generations. Even after wars end, food becomes abundant, fear leaves the body, and the marks of its existence remain scarred into the progressing populations. Warfare is never merely a present harm; its consequences seep into the future with the same destructive intent it inflicted upon the present. It is therefore imperative to recognise the perpetrators and root causes of such inhumane conditions, holding them accountable not only for the immediate suffering they unleash but for the inherited biological burdens they impose on future lifetimes.
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References
A global food crisis | World Food Programme. (2026). UN World Food Programme (WFP). https://www.wfp.org/global-hunger-crisis
GAZA STRIP: Famine confirmed in Gaza Governorate, projected to expand. (2026a). In Ipcinfo.org. https://www.ipcinfo.org/ipcinfo-website/countries-in-focus-archive/issue-134/en/
Action Against Hunger. (2026, May 7). The World’s Hungriest Countries | Action Against Hunger. https://www.actionagainsthunger.org/the-hunger-crisis/world-hunger-facts/the-worlds-hungriest-countries/
Peschansky, V. J., & Wahlestedt, C. (2013). Non-coding RNAs as direct and indirect modulators of epigenetic regulation. Epigenetics, 9(1), 3–12. https://doi.org/10.4161/epi.27473
Lacal, I., & Ventura, R. (2018). Epigenetic Inheritance: Concepts, mechanisms and perspectives. Frontiers in Molecular Neuroscience, 11, 292. https://doi.org/10.3389/fnmol.2018.00292
Winter, S., & Fischle, W. (2010). Epigenetic markers and their cross-talk. Essays in Biochemistry, 48(1), 45–61. https://doi.org/10.1042/bse0480045
Heijmans, B. T., Tobi, E. W., Stein, A. D., Putter, H., Blauw, G. J., Susser, E. S., Slagboom, P. E., & Lumey, L. H. (2008). Persistent epigenetic differences associated with prenatal exposure to famine in humans. Proceedings of the National Academy of Sciences, 105(44), 17046–17049. https://doi.org/10.1073/pnas.0806560105
Li, S., Wang, W., Zhang, D., Li, W., Lund, J., Kruse, T., Mengel-From, J., Christensen, K., & Tan, Q. (2021). Differential regulation of the DNA methylome in adults born during the Great Chinese Famine in 1959–1961. Genomics, 113(6), 3907–3918. https://doi.org/10.1016/j.ygeno.2021.09.018
Bender, A., Morel, M., Dumas, M., Klopfenstein, M., Osmani, N., Greenberg, M. V. C., Bourc’his, D., Ghyselinck, N. B., & Weber, M. (2025). UHRF2 mediates resistance to DNA methylation reprogramming in primordial germ cells. Nature Communications, 16(1), 7350. https://doi.org/10.1038/s41467-025-61954-0
