In an article by Eaton et al., it states that "although our genes have hardly changed, our culture has been transformed almost beyond recognition during the past 10,000 years, especially since the Industrial Revolution."1 We have strayed so far from our ancestral diets and lifestyles. Ancient peoples and even isolated hunter-gatherer cultures that still exist today ate wild, fresh foods in their natural state with minimal processing and certainly without synthetic chemicals. Their lifestyles were also very different from ours. According to another article by Eaton et al., "groups whose way of life tends to continue the Stone Age pattern have low rates of complex degenerative diseases." They did not suffer the same rates of degenerative diseases that plague modern society.
Findings from recent research suggests that the emerging middle classes from developing countries may as or more susceptible than western populations to obesity, type 2 diabetes and cardiovascular disease as a result of the chronic under-nutrition endured by their ancestors.
Led by Professor Anandwardhan Hardikar's team at the University of Sydney, the 12-year, multi-generational rat study suggests that because recent ancestors were exposed to chronic malnutrition, the populations' epigenetic makeup (whereby changing environmental factors alter how people's genes are expressed) has not compensated for these dietary changes.
"Their adverse metabolic state was not reversed by two generations of nutrient recuperation through a normal diet," said Hardikar. "Instead this newly prosperous population favoured storage of the excess nutrients as fat leading to increased obesity, cardiovascular disease and metabolic risk for diabetes when compared to their 'developed world' counterparts.
According to the team, this means their bodies are still designed to cope with undernourishment; so they store fat in a manner that makes them more prone to obesity and its resulting diseases than populations accustomed to several generations of a 'normal' diet.
This means that there will be a signficant impact from the cultural and socio-economic factors is now spurring the demand for convenience foods. If we place high priority on our health and understand that what we eat determines and shapes not just our physical characteristics but also our personalities as well, we’d all take what we eat much more seriously. Food even controls the very expression of our genes. We are connected to our food and where it comes from in ways that we have not yet fathomed and studies such as these are showing that we may not be able to correct the damage we are creating in one or even two generations.
The research team performed the multi-generational study on two groups of rats. The first group was undernourished for 50 generations and then put on a normal diet for two generations -- so mimicking the situation in many developing countries where recent increased prosperity has led to a sudden increase in calories -- from undernourished to a 'normal' diet.
Epigenetic changes in gene expression ultimately keep the risk of cardiovascular disorders higher than it would be had there been no exposure to unhealthy foods in the first place.
Quantifying epigenetic changes due to nutritional habits has been a challenge for scientists, but many are now stating the quest is even more important than acute bio-chemical reactions outside of the genome.
Meanwhile, the second (control) group maintained a normal diet for 52 generations.
At the end of the study it was found that when the descendants of the first group were exposed to a normal diet, this did not reverse the epigenetic modifications made by their undernourished forebears.
In fact, these rats were eight times more likely to develop diabetes and multiple metabolic defects when compared to the control group.
They concluded that eating a 'normal' diet can make animals, and possibly people, overweight, if their ancestors had been undernourished for several generations.
Biologists have suspected for years that some kind of epigenetic inheritance occurs at the cellular level. The different kinds of cells in our bodies provide an example. Skin cells and brain cells have different forms and functions, despite having exactly the same DNA. There must be mechanisms--other than DNA--that make sure skin cells stay skin cells when they divide.
The way we interact with the world changes our DNA, not just the other way around. More intriguing, one of the major ways we can change our DNA is by diet. For example, a study published in 2008 showed that exposing mice brains to as little as 6 hours of high blood sugar led to epigenetic changes that increased risk of vascular damage. These changes lasted even after 6 days of normal blood glucose, representing long-term damage after just a short blast of sugar. The research on long-term effects from short exposures is at the core of epigenetics. It’s furthered by data from another 2008 study published in the journal Diabetes.
Biomarkers of risk?
Hardikar also suggested that lower Vitamin B12 levels in the undernourished rats could also be an indicator of the trend -- a and is also something that has been suggested in humans.
"Human studies from Ranjan Yajnik's group at KEM Hospital in Pune, India have demonstrated that low circulating B12 and high folate levels are associated with insulin resistance and type 2 diabetes," he commented.
"Hopefully further research in understanding the gut microbes, which are major producers of Vitamin B12 in our body, and/or dietary supplementation with Vitamin B12 and other micronutrients, could reduce the risk of metabolic diseases in the coming generations," Hardikar added.
The ability of nutritional history to have durable affects on immune cells demonstrated in this new report could have profound implications for treatment of diseases with immune underpinnings.