“The secret to staying slim may be all in your genes,” the Daily Mail has today reported, adding that scientists have uncovered a “greedy gene that makes you eat more even when you are full”.
Before any dieters lose hope and reach for the nearest biscuit, it’s important to note that this news is based on research looking at a mutant gene in mice, not humans. The study examined the impact of a mutated gene called BDNF and the role it plays in telling the body it is full. Normally, various organs and tissues will use hormones to tell the brain that no more food is needed, causing the brain to suppress our appetite. However, when mice carried a mutant version of the BDNF hormone it appeared this fullness mechanism was blocked, which meant they carried on eating and gaining weight. Male mice carrying the mutation became nearly twice as heavy as their non-mutant counterparts, while females were 2.7 times heavier.
This study may provide a springboard for further research into the role of genetics in the development of obesity. However, this study was carried out in mice and the findings cannot be assumed to apply to humans, whose bodies may react differently to any similar mutation. It’s also not clear how many humans actually carry similar mutations, so it should not be assumed that all obesity is down to genetics.
Where did the story come from?
The study was carried out by researchers from Georgetown University Medical Center and the University of Colorado in the US. It was funded by the US National Institutes of Health and the American Diabetes Association.
The study was published in the peer-reviewed scientific journal Nature Medicine.
Generally, this research was covered well in the media, with the BBC and the Daily Mail emphasising that the study was carried out in mice, not humans. The Mail pointed out that even if the research leads to treatments for obesity, it will be years before these would be made available.
What kind of research was this?
This was an animal study that examined the role of a gene called “brain-derived neurotrophic factor” (BDNF) in the development of obesity. The researchers said that mutations of this gene have been shown to cause overeating and obesity in humans, and the researchers wanted to investigate how the gene influences energy balance.
The researchers said that energy balance is controlled by several organs that send signals to the brain when certain chemicals (such as the hormones leptin and insulin) are present in sufficient amounts. These signals cause several brain regions to react and control appetite and energy expenditure. The BDNF protein (which is generated using the BDNF gene in our DNA) is involved in regulating how signals are transmitted through the brain. Mutations within the BDNF gene can lead to a different form of BDNF protein being produced, potentially causing different effects compared with a typical form of BDNF.
Animal studies are often used to conduct early, experimental research and to examine specific interventions or processes before research can be carried out in humans.
What did the research involve?
The researchers took two groups of mice, one with a mutated version of the BDNF gene and the other with a normal version of the gene. They then monitored the eating habits of the mice, measuring the amount of food consumed as well as bodyweight and the development of obesity.
In order to uncover the mechanism by which BDNF mutations affect obesity, the researchers also studied the role of certain chemicals including the “hunger hormone” leptin and its ability to activate the hypothalamus and suppress eating behaviours. The hypothalamus is normally activated by leptin, although once activated the hormone suppresses the appetite. The researchers looked at the role of leptin in mice with and without the mutation, injecting them with leptin three times over a day. They then measured changes in eating habits throughout the day.
This animal study can provide information on the probable role of BDNF mutations on the development of obesity, but it cannot be assumed that the results apply to humans.
What were the basic results?
The researchers found that by five-to-six weeks of age, mice with mutated copies of the BDNF gene developed severe obesity and had a higher body weight than mice that did not have a mutated version of the gene.
By 16 weeks of age, female mice with the mutation were 171% heavier than their non-BDNF mutation counterparts, and male mice were 90% heavier. The researchers found that the obesity was caused by eating more food, not reduced activity levels. They found that the mice carrying a mutated version of BDNF ate 69%-80% more food than their counterparts.
When examining the role of leptin in the regulation of eating in mutant mice, the researchers found that the chemical did not activate the hypothalamus and inhibit eating as it does in mice without a mutated version of BDNF. They found that the mice that did not carry a mutated version of BDNF reduced the amount of food they ate by 26% after being injected with leptin. The mice with the mutated form of BDNF, however, showed no changes in the amount of food they consumed after having leptin injections.
How did the researchers interpret the results?
The researchers concluded that mutations of the BDNF gene caused obesity due to overeating. They further concluded that, in mice carrying this mutation, leptin’s ability to activate the hypothalamus and regulate food consumption was impaired.
This study shows that BDNF mutations can cause obesity in mice and suggests a possible mechanism through which it might work. However, while it may lead to further investigations into the role of this gene in human obesity, the results cannot be directly applied to people. Firstly, the biological mechanisms and processes involved may not apply to the human body, and even if they did, human hunger and eating is unlikely to be solely influenced by a single mutation, with factors such as willpower and environment also involved. It is also not clear how many people carry the gene and whether it is found in a high proportion of obese people.
The researchers say that understanding the way in which communication circuits in the brain have an effect on energy balance and eating habits could lead to new strategies for addressing or treating obesity. However, the current study is at a very early stage, and is unlikely to lead to such strategies in the near future.
Several factors can contribute to the development of obesity in humans, including high food intake, low activity levels, genetics and socioeconomic factors. While research into the genetic factors that contribute to obesity is informative and may lead to the development of treatment options, there are strategies available now to treat obesity, such as exercising more and eating a healthy balanced diet high in fruit and vegetables and lower in sugars and saturated fats.
Analysis by Bazian