The idea of eating a tub of ice cream to cope with being upset has become a bit cliche. Though some might not need a tub of chocolate swirl to help perk themselves up again, there do seem to be systematic differences in the way that people cope with upsetting events, with some more likely to find solace in food than others. Continue reading
Your body mass index (BMI) indicates whether you are within a healthy weight range based on your height. Having a higher BMI – meaning more weight relative to height – can increase your risk of developing heart disease, cancer and type 2 diabetes. While BMI is partly determined by your environment and lifestyle – including your diet and how much you exercise – our genes also play a role.
Genes are inherited from our parents. When this genetic information from the egg and sperm combine, the DNA is replicated continuously – doubling the number of cells until an entire baby is formed. DNA replication is not perfect and every single base in the human genome – the single blocks of code which make up entire DNA strand – has the potential to be mutated for good or for bad. Importantly, this creates a huge amount of random genetic variation at a population level, which is like a huge natural genetic experiment. If we know that these random genetic changes are linked to small changes in BMI, we can test whether BMI influences lots of different things, including cardiovascular health – like a randomized controlled trial.
Broadly, there are two ways of identifying parts of our DNA which are linked with particular traits. Studies of patients affected by rare obesity-related disorders (candidate gene studies) or large-scale population-based genome-wide association studies (GWAS). Findings from the latter of these methods – studies that look to see whether a change at any position in our DNA is linked with a particular trait – have implicated hundreds of common genetic variants associated with BMI.
A 2015 study conducted by the Genetic Investigation of Anthropometric Traits (GIANT) consortium and published in Nature found 97 places in our DNA which influence BMI levels and which were responsible for small differences between people, regardless of how different their environment and lifestyles were. This means that, while we cannot predict an individual’s BMI with genetics, we can refer to genetics to understand if patterns materialise in populations.
Small, genetically driven changes in BMI provide an opportunity to determine whether differences in BMI between people have a role in health and disease. Genetic mutations which are randomly allocated at conception aren’t easily changed by our environment and experiences later in life. As a result, our BMI, weight and chances of developing obesity-related diseases could partly be determined before we’re even born.
Low BMI, low heart disease risk
Using this property of genetic variation, we undertook a study that was recently published in the scientific journal Circulation. Our research showed that higher BMI is likely to have an influence on measures of cardiovascular health, such as blood pressure, in more than 3,000 healthy 17-year olds from the Avon Longitudinal Study of Parents and Children (also known as the Children of the 90s).
The Children of the 90s study, based in Bristol, has followed families in the UK through data collected from questionnaires, clinics and biological samples since the early 1990s. Using MRI scans from 400 21-year old Children of the 90s participants, who were recruited based on genetically driven differences in BMI, we also demonstrated that having a higher BMI is likely to lead to structural damage to heart tissue, including an enlarged left ventricle – the heart’s main pumping chamber.
Until now, studies have typically looked at the link between BMI and cardiovascular health in adults by observing patterns within populations. However, it’s difficult to conclude a relationship between the two without confusing the role that lifestyle factors play or finding how cardiovascular disease changes BMI rather than the reverse. Surveying people is also open to many sources of bias, such as recalling or reporting information incorrectly.
We wanted to isolate the property of genetic variation to improve our confidence in drawing conclusions about the relationship between BMI and cardiovascular health in a population of healthy young people.
Our results support the idea that having a healthy, normal BMI from a young age is likely to maintain a healthy cardiovascular system and help prevent heart disease later in life. Modern genetics allow us to investigate the causes of disease more quickly and cheaply than ever before, and the availability of genetic data in studies such as the Children of the 90s means we can more readily overcome limitations of traditional studies. We hope these findings lead to increased efforts to tackle the obesity epidemic at all stages of life, starting in early age.
Dr Laura Johnson, Senior Lecturer in the Centre for Exercise, Nutrition and Health Sciences, discusses her new paper in which she assesses the impact of dietary patterns on obesity and how modelling may help influence change in both personal habits and public policy.
No single food or nutrient is to blame for obesity. There so many routes from diet to overeating and weight gain, and in real life foods and nutrients aren’t eaten on their own. So, it’s misleading to look at foods that way in research, it’s the overall balance of diet that matters. Continue reading
I come from Crete. I grew up in a house where everything revolved around the kitchen. Most of my childhood memories involve my mother preparing meals from scratch, using olive oil. Meals were accompanied with vegetables and we had a legume soup (like lentils, beans, chickpeas) twice a week. All of them were a pleasure to eat; they just needed olive oil and a slice of bread to scoop up the juices to receive a cook’s highest reward: empty plates.
I’ve lived in the UK for 10 years and I still can’t enjoy vegetables or salad unless I prepare them myself. They are boiled and boring, with uninspiring dressings, and no tomato sauce or sautéing with olive oil and onions to give them some flavour. It’s no wonder that 70% of adults in the UK do not eat enough fruits and vegetables and that on average they consume 14g of legumes a day (half the amount consumed in the traditional diet of Crete).
Last month’s government-commissioned school food review showed that the nutritional quality of school food has improved substantially since 2005, when Jamie Oliver started its campaign to improve the nutritional value of school meals. Nevertheless, take-up of school meals remains low, at 43%. In other words, 57% of children are not eating school lunches, but bring a packed lunch, have snacks, or buy their food elsewhere. The report shows that the majority of these meals are unhealthy. In fact, in contrast to what most parents think, only 1% of packed lunches meet the nutritional standards.
In addition to affecting child health, there is substantial evidence that poor nutrition affects cognitive performance. Michèle Belot and Jonathan James show in their study that the Jamie Oliver campaign led to a significant increase in children’s test scores in primary schools (Key Stage 2), as well as a drop in authorised absences (i.e. those that are mostly linked to illness and health).