The old saying goes, “You are what you eat,” but recent findings from Tulane University suggest that deficiencies in one’s diet might affect not only one but also future generations’ health.
Emerging research has long supported the notion that famines affecting one generation can have detrimental genetic repercussions for the following one. However, the depth of these effects across multiple generations has remained a question, particularly under conditions of nutritional adversity.
A pivotal study conducted by Tulane University and published in the journal Heliyon provides new insights. The research involved pairs of mice subjected to a low-protein diet, and the findings were concerning: over the next four generations, the offspring exhibited significantly reduced birth weights and smaller kidneys—leading indicators for chronic kidney disease and hypertension.
The study highlighted a persistent issue: Even when dietary interventions were made in the offspring, there was no positive alteration in outcomes. Subsequent generations continued to display low nephron counts—a crucial component of the kidneys responsible for filtering waste from the blood. While more research is needed to confirm if these findings apply to humans, they highlight the enduring impact that food insecurity and malnutrition could have on health outcomes spanning decades.
The lead researcher, Giovane Tortelote, an assistant professor of paediatric nephrology at Tulane University School of Medicine, likened the situation to an avalanche. He noted that despite dietary corrections in the first generation, the following generations—up to the great-great-grandchildren—might still suffer from lower birth weights and reduced nephron counts, even if they never experienced direct starvation or protein-deficient diets.
Interestingly, the study also showed that these transgenerational effects occurred regardless of whether the mother or the father had a deficient diet, underscoring the role of maternal and paternal nutrition in fetal development. This introduces a novel aspect to epigenetics, which examines how environmental factors influence gene expression without altering the DNA sequence.
Further observations from the research indicated that by the third and fourth generations, nephron counts in offspring began to approach normal levels, although it remains unclear which generation might fully revert to standard kidney development. The mechanisms behind this potential reversal are yet to be understood. Tortelote emphasised the need for additional research to pinpoint the exact generational shift where normal kidney development resumes and to understand why these traits are passed down initially.
The study not only sheds light on the mechanisms that could be contributing to chronic kidney disease—a significant cause of death in the U.S.—but also the vicious cycle of hypertension and kidney damage it entails. This underscores the public health crisis that could affect populations for decades, mirroring human life spans.
With these findings, two critical questions emerge: is it possible to reverse these effects, and if so, how? These questions highlight the urgent need for strategies to address and mitigate the long-term health impacts of dietary deficiencies across generations, presenting a profound challenge for public health policy and medical research moving forward.
More information: Fabiola Diniz et al, Morphometric analysis of the intergenerational effects of protein restriction on nephron endowment in mice, Heliyon. DOI: 10.1016/j.heliyon.2024.e39552
Journal information: Heliyon Provided by Tulane University
