Obesity Worldwide has More than Doubled Since 1980

Obesity worldwide has more than doubled since 1980. In 2014 more than 1.9 billion adults were overweight and more than 600 million were obese according to the World Health Organization. This trend is showing no sign of slowing, in fact, with more and more children becoming obese at even earlier ages it seems that obesity is going to be one of, if not the greatest challenge that society will face in the 21st century.

In spite of the escalating problem, our understanding of why some people will become obese and why others who live in a similar environment will not is limited. It is clear that the brain plays some role, but this role is not yet fully understood. Meanwhile, lifestyle choices may play some part, but cannot explain everything. After all, for some of us it is relatively easy to live healthily, whilst for others it is problematic and nigh impossible.

However, there has recently been a breakthrough in our understanding of obesity. Research from scientists at Baylor College of Medicine, the National Institutes of Health and Virginia Tech Carilion Research Institute can help us to further understand obesity and even offers hope that it may be treatable. The scientists, chief among them Dr. Makoto Fukuda, have been studying mice and they have made some very significant discoveries. Their findings are primarily concerned with the ‘Rap1 gene’. This gene is involved in many parts of the body, including the brain where it plays a role in learning and memory.

During their research, the scientists genetically engineered mice so that they did not have the Rap1 gene. They put these mice on an unhealthy, high fat diet along with a control group of normal mice. Whilst the normal mice put on a lot of weight, the mice lacking the Rap1 gene did not, as they ended up choosing to eat less than the control group. Essentially, their hypothalamus would produce more of a hormone called POMC which reduces the appetite. These mice also ended up with lower levels of blood glucose and insulin than mice from the control group.

Dr Fukuda and his colleagues also studied how the Rap1 gene affects the hormone ‘leptin’. This is essentially the hormone that tells us we are full and do not need to eat any more. Obese people still produce leptin, but they become resistant to it, so it does not stop them from eating more than they should. Essentially it can be a downhill spiral with people eating more unhealthy food and consequently reducing their ability to tell that they are full. Returning to the mice, those lacking the Rap1 gene did not develop decreased sensitivity to leptin, despite eating a ‘modern’ high fat diet.

The researchers were also interested in whether the effects of reducing Rap1 could be imitated using a drug. They tested this using ESI-05 on obese mice. To their delight the mice responded by eating less and reducing their weight, giving hope that obesity may become treatable in the future.

While more research is needed into the role of the brain in obesity, the results of this and any further studies may have huge implications on our ability to take the upper hand in the struggle against a problem that until now has shown no signs slowing down.

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