Poverty has become an immense problem in not just the United States, but all over the world. Because people can’t afford proper medical care or means to follow a nutritious diet, they often experience poor health. Being unwell can then result in not being able to earn a sufficient income, creating a vicious cycle that can lead to a slew of financial and health-related issues.
Our health is the most important thing to us. We only get one body, and it is eminent that we take care of it properly. Although diet and exercise are essential for maintaining a healthy lifestyle, it turns out that socioeconomic status (SES) also factors into health and associates with the activity of our genes, or our epigenetics. Exactly how SES epigenetically links to overall wellbeing, however, is not fully understood.
In a recent study out of Northwestern University, Dr. Thomas McDade led a team of researchers on the journey into discovering the effect that poverty can have on a person’s genome.
Using whole-genome analysis, the team set out to discover the underlying mechanisms that are responsible for the relationship between SES and health. They evaluated leukocytes obtained from the Cebu Longitudinal Health and Nutrition Survey of 489 Filipino participants of different incomes, educations and living situations.
They found that living in poverty can affect DNA methylation levels on the genome, and leave a person susceptible to developing health problems later in life. We’ve previously seen that poor SES may have an epigenetic link to developing depression, but it may also lead to insulin resistance, chronic inflammation, and a whole other string of health problems.
DNA methylation is an important epigenetic mechanism that helps regulate gene expression. It involves the addition of methyl groups to the 5th cytosine base of DNA, and it often results in gene silencing. Increased DNA methylation in specific regions is often a product of high-stress environments, making this epigenetic mark an obvious starting point.
Evidence from the study showed that people who live in poverty experience higher levels of DNA methylation— approximately 2500 CpG sites over 1500 genes, which works out to be just about 10 percent of the genes in the genome. Genes associated with increased DNA methylation were related to skeletal development, immune response and neurological development, demonstrating the cause for future health concerns.
Dr. McDade was surprised to learn that connection between SES and DNA methylation was so overbearing, and highlights the importance of their findings. “First, we have known for a long time that SES is a powerful determinant of health, but the underlying mechanisms through which our bodies ‘remember’ the experiences of poverty are not known”. He continued to explain that poverty can contribute to altering the architecture of the genome, which could result in changing the way the human body functions.
McDade hopes that future studies can determine the exact effects of methylation at different genes. “Our findings suggest that DNA methylation may play an important role, and the wide scope of the associations between SES and DNAm is consistent with the wide range of biological systems and health outcomes we know to be shaped by SES”, he said, pointing out that our life experiences become embodied in our genome. The methylation sites uncovered by the researchers will need to be further evaluated, but most are linked to immunity, skeletal growth, and the nervous system.
Poverty is and has been an epidemic for quite a while. This study provided valuable insights into the mechanisms behind the relationship between poor health and SES. Hopefully, further research can help take step towards ending poverty and ensuring a quality life for everyone.
Source: McDade T. et al (2019). Genome‐wide analysis of DNA methylation in relation to socioeconomic status during development and early adulthood. Am J Phys Anthropol. 169: 3–11.
Reference: Hilary Hurd Anyaso, Northwestern Now, Poverty leaves a mark on our genes Northwestern University, April 05, 2019.