The DNA that is stored in every cell in your body isn’t the end-all be-all of your genetic identity that many people assume. While it’s impossible to change the hardwired sequences stored in every cell’s nucleus – ignoring the developing field of gene therapy – the way that genetic data expresses itself is highly variable.
DNA in and of itself doesn’t really do anything. It’s the bits and pieces of molecular machinery between the DNA’s instructions and the final product of constructed proteins that do the actual work. Different types of RNA, tons of enzymes, ribosomes, and amino acid building blocks are constantly churning out the basic complexes that keep your body running. Which sections of DNA are providing life’s blueprints and how those instructions are carried out depends greatly on what’s happening to you on a macroscopic level.
Depending on your health and life’s conditions, your genes can express themselves in different ways. Small changes such as the amount of sunlight your skin receives, the amount of food you have access to, and the relationships you enjoy amongst your peers all have subtle to major effects on the realization of your genetic code. The study of these factors and how they affect you is called epigenetics.
But epigenetics and do more than just affect your life; it can also affect your offspring. Men’s sperm is constantly dividing in their testicles, and you can bet that the way a man is living his lift affects how those little soldiers are produced. Which genes get passed on and the rate of errors copying them down is not set in stone. Perhaps even more variable is the conditions of the woman’s life while the fetus is developing. Not only does environment change the way her body is behaving, it affects the very earliest genetic activation in a child.
One prime example of this that has played out in the real world is in a small Swedish town called Overkalix. Thanks to detailed records of crop harvests and direct male lineages, a fascinating study of epigenetics and longevity was able to be completed. The small northernmost county in Sweden saw many alternating periods of feasting and famine. Lars Olov Bygren, a preventative health and nutrition researcher at Sweden’s Karolinska Institute, can trace his ancestry in the village all the way back to 1475.
He also realized that the raw amount of data made for a perfect study opportunity.
Boys who experienced a year of feast just before they reached puberty – a time when sperm cells are maturing – had offspring who died an average of six years earlier than forefathers who reached puberty during famine times. The children and grandchildren of “feast” fathers had greater instances of diabetes, heart disease, and many other illnesses.
So if you want your children and grandchildren to live a long, healthy live, you should starve yourself just before puberty. But more importantly, the study goes to show just how important living conditions can be to epigenetics.
In a more recent study from the Ohio State University, Richard Steckel, distinguished university professor of economics, anthropology, and history, thought a similar phenomenon might be happening in the American South. According to the “thrifty phenotype” hypothesis, children born into poverty who gain greater access to food later in life are ill-equipped to biologically handle the extra calories. This leads to an excess of people with obesity and type 2 diabetes.
So, for example, in the American South, the black population had a pretty rough go of it up until the 1950s. But once industrialization took hold leading to rapid economic growth for more than three decades, access to calorie-dense, processed foods shot through the roof, right when their bodies were least prepared to handle it. Seeing as how African-Americans are more susceptible to diabetes to begin with, this led to rates near epidemic proportions. And no, that’s not being racist. That’s just genetic fact and population fact. Check out the map mentioned above.
To test this hypothesis, Steckel turned to statistics. He analyzed a map outlining type 2 diabetes prevalence throughout the United States, obtained state per-capita income data, and constructed a statistical model to investigate the consequences of income change on diabetes prevalence. The model suggested that two variables, the income ratio between the 1950s and today and the share of each state’s population that was African American in 2010, could explain more than half of the nation’s variance in the prevalence of Type 2 diabetes.
Of course, that’s not the entire story. Industrialization also made the population more sedentary, changing how people worked and what they had to do to be comfortable at home. Children are also playing outside less and leading more of a video game lifestyle. But at least some of the diabetes rate can be blamed on epigenetics. People’s bodies were primed for a life of starvation, but instead came into a world full of Rally’s thickburgers.
The study, “The hidden cost of moving up: Type 2 diabetes and the escape from persistent poverty in the American South,” was published in the American Journal of Human Biology by the aforementioned Richard Steckel.