“You are what you eat” may be a truism but you may also be what your parents ate too. This is important because despite genetics contributing to health and disease, so does environment and although we can change our environments for the better, we were most susceptible to environment during the first 1,000 days of our lives.

This exciting and growing field is called the “Developmental Origins of Health and Disease” or DOHaD for short. It even has its own journal. This blog summarises some of the papers from a recent special issue. It highlights work on the mechanisms of the developmental origins of health and disease and the use of animal and human studies of how we should modify our environment to lessen the chance of chronic diseases such as obesity, which increases risk of type 2 diabetes, heart attacks and stroke.

Ngo and Sheppard from Auckland, New Zealand, focus on a tiny molecule with a huge role. The addition of a ‘methyl’ molecule (one carbon and three hydrogens) to DNA can change the way it acts without changing its DNA sequence. This is called epigenetics. Reviewing the literature, the authors conclude that after a gene gets turned off, it needs methyl molecules added to ensure it doesn’t accidentally get re-activated. Think of it as locking a door that has just been closed.

Ong, Lin and Holbrook from Singapore, review the best ways to analyse the methyl molecule. Most importantly, they summarise recent studies that have overturned the way we think about genes and environment. Up to now, most studies have looked at genes or environment but seminal work from the authors and others has indicated that we must analyse genes and environment because most of the time, they act together. Only by understanding both can we can move towards calculating people’s risk factors for disease, which will lead to more personalised prevention and treatment.

Toop and colleagues from Adelaide, Australia, focus on how and why added sugar, mainly from sugary drinks, is bad for mothers of young children. Working with rats, they compare how maternal consumption of common sugar or corn syrup affect the mother and offspring. Of the two, corn syrup is considered the most dangerous because it contains more fructose, a sugar that can literally go straight to your liver and start making fat. Governments are so worried by both types of sugar because they increase the risk of illness during pregnancy such as gestational diabetes and increase the likelihood of premature birth and a heavier birth weight, all of which predispose to obesity and type 2 diabetes. Current recommendations are for to limit consumption to less than one sugary drink per day. In this paper, researchers found that both sugars, when consumed at levels similar to those consumed by humans in pregnancy and during breastfeeding, had a negative impact on measures associated with risk for diabetes. However, common sugar had a worse effect than corn syrup, putting mother rats off their normal food and increasing their body fat, cholesterol and shrinking their livers. More studies are needed in to see if the situation is similar in humans.

Karmali and colleagues turned their attention to humans, specifically Indians who had migrated to The Netherlands. Back in India, it is common for babies to be born “thin-fat”, lighter than average but with more brown fat – the type of fat that provides the most energy. This combination predisposes to obesity and type 2 diabetes. It was previously thought that those who migrate to other countries can change their disease susceptibility by changing their diet to that of their host country. However, researchers found that those born in The Netherlands to Indian parents were also “thin-fat”. They concluded that, as with the finding of Ong and colleagues, that the interaction of genetics with environment must also play a major role in disease risk in migrants and most likely the rest of us.

Finally, Madsen and colleagues from India, Denmark and the UK, reported on a simple fitness intervention in young men in India. They found that regular cycling increased physical fitness and blood-based markers of risk for type 2 diabetes.

The take-home message: we all need a healthy start to life to optimise the way our genes work but it’s never too late to change your genes.

Access the above papers published in Journal of the Developmental Origins of Health and Disease, without charge until 31 May 2015, via this link: http://journals.cambridge.org/doh/epi15

We have also included recently published articles on Epigenetics published in JDOHaD



  1. Most of the medical students I teach are not familiar with the DOHaD construct. It is really important if they are to help their future patients understand the primary prevention aspects of DOHaD

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