How our environment influences our genes, sometimes for generations into the future, is one of the hot new frontiers in nutrition research. The field is called epigenetics, and in this blog post, Dr Phil Parker gives his insights into evolving research.
Epigenetics describes chemical factors that affect the expression of DNA that makes up our genes. While genetics refers to the gene sequence, or DNA code, epigenetics refers to all the other factors that control how and when each gene is expressed.
A person’s ‘epigenome’ can be altered by a variety of factors including environmental pollution (such as BPA in plastic affecting our epigenomes), stress, disease and nutrition. Importantly, these epigenetic factors can become heritable. This really does mean that you are what your mother (and grandmother) ate, slept, breathed and felt!
In a just released study, researchers compared the epigenetic methylation profile in women who are obese, formerly-obese (following gastric-bypass surgery) or never-obese. Methylation of DNA can be thought of as putting up concrete barricades on an airport runway – the methyl groups prevent the enzymes that turn DNA into protein from landing and doing their job. The authors focused on the methylation of genes involved in adipogenesis (creation of new fat cells) partly explaining the increase in fat-cell numbers observed in obese adults compared to never-obese adults – an increase that remains even after weight-loss.
Hyper-methylation of DNA stops the production of proteins coded for by genes. Conversely, hypo-methylation (the focus of the current research study) allows the DNA code to be turned into a protein product. Turning on or off genes by methylation is not always a bad thing. Methylation is a common way in which the body controls specific gene expression (and thus the phenotype) of every cell in the body.
It is methylation that is used to turn specific genes on and off giving each of us our sex whilst in utero. However, aberrant methylation of genes (either hyper- or hypo-) can certainly affect the proper functioning of cells and is becoming increasingly studied in a variety of diseases including cancer, obesity and mental-health.
The current study found increased hypo-methylation (allowing gene-expression) in obese and formally-obese women compared to those who were never-obese. Interestingly, hypo-methylation did not translate into altered gene expression in post-obese women, compared to the never-obese group. However, hypo-methylation of the same genes in currently-obese women did result in an altered gene-expression profile, suggesting that overfeeding or weight gain may be a necessary additional step to triggering adipocyte hyperplasia.
What are the potential consequences of this hypo-methylation in formerly-obese women? Well, it indicates a significant alteration in the normal functioning of adipocytes in women who have gained weight.
Our adipocytes communicate directly with our liver and affect the proper (or not) functioning of our entire body. These changes remain even after the weight has been lost and may help explain the persistent differences in disease profiles and the propensity to regain weight in women who were formerly obese, as compared to those who were never obese. Preventing obesity (particularly in children) is key!
There were a number of limitations within the study design that were acknowledged by the authors. These include sample numbers and a lack of investigating into differences between women who have lost weight following bariatric surgery compared to a lifestyle intervention. However, information from this work represents a very interesting and worthwhile investigation into the epigenetic profiles of obese, formerly-obese and never-obese women and the effects these differences may have on health and on the ability to maintain a healthy weight.
Dr Phillip Parker, Deakin University