The Effects of Poor Eating Habits On The Immune System Last Long After Diet Improves
While we may be familiar with the dangers of eating too much processed foods, the actual effects of this indulgence may be far more damaging to our health than previously imagined. Almost everyone knows that improved eating habits will most likely improve a range of health measures, but researchers have warned that the effects that a poor diet have on the immune system can persist even after eating habits improve.
Writing in the Journal of Leukocyte Biology, the team behind the new study found that even after successful treatment of atherosclerosis - including lowering of blood cholesterol and a change in dietary habits - the effects of an unhealthy lifestyle still affect the way the immune system functions.
Led by Erik van Kampen from Leiden University in The Netherlands, the researchers used a mouse model to show that lasting changes in immune functions occurs largely because poor eating habits alter the way genes express themselves, including genes related to immunity.
The Study of Epigenetic Changes Is Paramount
These 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, said the team.
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.
"We've long known that lifestyle and nutrition could affect immune system function," commented John Wherry, Ph.D., deputy editor of the Journal of Leukocyte Biology.
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.
Our genes are located on twisted, double-stranded molecules of DNA called chromosomes. At the ends of the chromosomes are stretches of DNA called telomeres. These are essentially end caps that protect our genetic data, allow for cells to divide properly and reflect how we age. High blood glucose may damage our telomeres; the ends of our DNA code. Considering that an undamaged telomere may be protective against cancer, death, and the very act of aging, any process that harms telomeres could put us at substantial risk.
"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," he said -- adding that research to investigate the length of such effects will be 'critical.'
"I hope that this study demonstrates the importance of diet-induced changes in the epigenome and encourages further research into the interaction between dietary patterns, DNA methylation and disease," added van Kampen.
The team analysed two groups of mice that had an altered gene making them more susceptible to developing high blood cholesterol and atherosclerosis. These mice were either fed a high-fat, high-cholesterol diet (Western-type diet, WTD) or a normal diet (chow).
After a long period of feeding, bone marrow was taken from the mice and transplanted into mice with a similar genetic background that had their own bone marrow destroyed. The recipient mice were left on chow diet for several months, after which the development of atherosclerosis in the heart was measured.
Van Kampen and his colleagues then examined the number and status of immune cells throughout the body in addition to analysing epigenetic markings on the DNA in the bone marrow.
They found that DNA methylation, an epigenetic signature, in the bone marrow was different in mice that received bone marrow from the Western-type-fed donors compared to the mice receiving bone marrow from chow-fed donors.
In addition, these mice had large differences in their immune system and increased atherosclerosis, said the team.
"We conclude that WTD challenge induces transplantable epigenetic changes in bone marrow, alterations in the hematopoietic system, and increased susceptibility to atherosclerosis," concluded the team.