New insights into the heightened risk of prostate cancer in the offspring of malnourished pregnant women have emerged from rat experiments conducted by researchers at São Paulo State University (UNESP) in Brazil. Two studies, published in Scientific Reports and Molecular and Cellular Endocrinology, shed light on the gene expression alterations and hormone imbalances that contribute to the increased susceptibility to prostate cancer later in life.
Study Findings:
In the first study published in Scientific Reports, researchers identified gene expression alterations associated with hormone imbalances observed in rats’ offspring. The lack of protein during gestation and lactation was found to disrupt molecular pathways crucial for normal prostate development, with over 700 genes affected, including the ABCG1 gene linked to prostate cancer.
According to Professor Luis Antônio Justulin Junior, leading the research at the Botucatu Institute of Biosciences (IBB-UNESP), a protein-poor diet during the embryo stage and the initial two years post-birth significantly influences gene expression. This revelation underscores the lifelong impact of nutritional choices during crucial developmental stages.
In the second study, published in Molecular and Cellular Endocrinology, researchers identified deregulation of microRNA-206, correlating with an early-life increase in estrogen levels in the offspring of female rats subjected to a protein-restricted diet during gestation and lactation. Elevated estrogen is a recognized factor associated with a higher risk of prostate cancer.
Understanding the First 1,000 Days:
Professor Justulin emphasized the importance of these findings in understanding the critical period of the first 1,000 days of life, encompassing pregnancy, breastfeeding, and infancy until the baby’s second birthday. The research contributes to the growing field of developmental origins of health and disease (DOHaD), exploring the profound impact of gene-environment interactions during early developmental stages on the lifelong risk of non-communicable chronic diseases.
Epigenetics and Lifelong Impact:
The study aligns with the broader field of epigenetics, focusing on how behavioral and environmental factors, particularly maternal malnutrition, influence gene expression. Epigenetic changes, reversible alterations that don’t mutate DNA sequences, can shape an organism’s reading of DNA and impact gene expression in subsequent generations. The UNESP research delves into cellular mechanisms through rat experiments, unveiling critical insights into the complex interplay between nutrition, gene expression, and prostate cancer risk.
Conclusion:
These UNESP studies underscore the profound link between maternal nutrition, gene expression, and the lifelong risk of diseases such as prostate cancer in offspring. The findings highlight the urgency of understanding and promoting optimal nutritional practices during critical developmental windows, offering potential avenues for mitigating long-term health risks.
