Professor Jeffrey Friedman (centre) receives the
UCL Prize Lecture in Clinical Science Medal from
UCL President and Provost, Professor Malcolm
Grant (right), and Professor Tony Segal.

Written by guest blogger, Marianne Neary, MBPhD student

Yesterday  a group of UCL MB PhD students met Professor Jeffrey Friedman for afternoon tea in the Wilkins Terrace restaurant.  We were granted the honour of a private audience before his UCL Prize Lecture in Clinical Science.

In 1994 Professor Friedman, and his colleagues at the Rockefeller in New York, made a landmark discovery which armed obesity researchers with a new weapon in the battle against widening waistlines and burgeoning bum-prints.

It saw the dawn of obesity genetics as Professor Friedman and his team identified the ‘obese’ (ob) gene in mice and humans. This gene codes for a hormone he later named leptin.

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What drives the differences? © Nutrition Reviews

King’s College London’s Tim Spector, as he told his audience at the Cheltenham Science Festival, used to hold the view that “everything is genetic”. Our genes are an important and complex part of determining who we are – our appearance, behaviour and susceptibility to disease.

We know, too, that our day-to-day environment and random chance also influence how we develop: how many pairs of identical twins do you know who look and act exactly the same?

But Professor Spector has since changed his point of view. There’s a third element – epigenetics – that helps to shape the differences between identical twins, and between all of us. We’re increasingly seeing how important it may be.

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Gail Davies (UCL Geography) travels around the world looking at laboratory mice, and the scientists who study them. To find out why a geographer would be spending her life doing this, I went to hear her in conversation with Steve Cross – Head of UCL’s Public Engagement Unit (and a closet geneticist) – at the event Mice People: Cultures of Science organised as part of the Humanimals season at the UCL Grant Museum of Zoology.

Gail is a human geographer interested in how science works, both in terms of the interface between nature and culture, and the spatial aspects of science.

A big part of her work is looking at how science varies internationally. Taking an extremely broad view of science, there have been two big “science migrations”. The first was after World War II when many European scientists moved to America. The second is happening now, with a huge shift in science going towards south-east Asia.

However, scientists don’t move around the globe alone. In the case of quite a few biologists, they take their mice with them. In fact, as Gail explained, if you take away apparatus, knowledge of standard methods etc., “the international knowledge economy looks rather furry”.

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Professor Steve Humphries (UCL Institute of Human Genetics and Health) delivered an insightful and comprehensive Lunch Hour Lecture, on 23 February, regarding the issues surrounding genetic testing for risk of heart disease.

The lecture was broken down into four manageable chunks: (1) The causes and mechanisms of heart disease (2) What is a gene? (3) What is SNP and how is it useful? (4) How can we use DNA tests?

The causes and mechanisms of heart disease
To begin the lecture Professor Humphries challenged the audience to suggest known risk factors for heart disease. This was effective in engaging the audience and a wide-ranging list was compiled, including: high blood pressure, obesity, smoking, diabetes, age and male gender. The risk factors could be genetic or environmental, but in reality, many are a combination of both.

Professor Humphries then proceeded to explain briefly the mechanisms of heart disease illustrating his points with some supportive graphics.

To summarise, he described the fact that after being born with clean arteries there can be the process of ‘silent build up’, which takes place in early adulthood. Although this can be reversed, in many it will lead on to fatty streaks, atherosclerotic plaques and in the unfortunate; chest pain, plaque rupture and myocardial infarction.

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