Genetics is known to influence food cravings, with carriers of a particular version of the FTO gene seemingly biologically wired to eat more and feel hungrier sooner. In ancient humanity, where food was scarce, this is likely to have been a straightforward survival mechanism, but it becomes problematic in a modern world with easy access to high-energy foods. Your FitnessGenes result will tell you whether you have any copies of the FTO gene linked to increased appetite.


The relationship between the genetic variations in FTO, diet, and body composition is very complex. There is much research still to be done. We are contributing original knowledge to this area through our collaboration with Loughborough University and University College London (http://www.lboro.ac.uk/news-events/news/2015/march/obesity-gene.html) . Thank you to everyone who has helped further this research by completing our survey!

Losing those few extra pounds can often be a struggle, and some of us certainly find it harder to shift the fat than others. An increase in the levels of obesity worldwide over the past 20 years clearly puts the blame on the rise in access to cheap, easy calories such as those found in convenience and fast food.

However, we are increasingly beginning to understand that genetics also has a role to play in why some of us find it harder to lose weight than others. One classic study compared the weight of over 500 adopted children with their biological parents, and also their adoptive parents. If family environment was more important to the children’s weight then you might expect to find a closer match to the adoptive parents. What the researchers actually found was that the children’s weight was much more similar to the weight of their biological parents.

We now know that a number of different genes play an important role in determining how much you weigh throughout your life. The involvement of genetic factors in the development of obesity is estimated to be between 64—84%. One of the strongest associations is with a gene known as FTO.

Global population distribution:

Source: 1000 Genome Project. Global averages for both sexes

FTO: AA

14%

FTO: TA

40%

FTO: TT

46%

More about FTO

LEARN MORE ABOUT FTO: A GENE FOR APPETITE

The relationship between the genetic variations in FTO, diet, and body composition is very complex. There is much research still to be done. We are contributing original knowledge to this area through our collaboration with Loughborough University and University College London (http://www.lboro.ac.uk/news-events/news/2015/march/obesity-gene.html) . Thank you to everyone who has helped further this research by completing our survey!

Losing those few extra pounds can often be a struggle, and some of us certainly find it harder to shift the fat than others. An increase in the levels of obesity worldwide over the past 20 years clearly puts the blame on the rise in access to cheap, easy calories such as those found in convenience and fast food.

However, we are increasingly beginning to understand that genetics also has a role to play in why some of us find it harder to lose weight than others. One classic study compared the weight of over 500 adopted children with their biological parents, and also their adoptive parents. If family environment was more important to the children’s weight then you might expect to find a closer match to the adoptive parents. What the researchers actually found was that the children’s weight was much more similar to the weight of their biological parents.

We now know that a number of different genes play an important role in determining how much you weigh throughout your life. The involvement of genetic factors in the development of obesity is estimated to be between 64—84%. One of the strongest associations is with a gene known as FTO.

FIRST WORLD PROBLEMS: OBESITY

Obesity is currently one of the biggest health challenges we face. At the latest count, the World Health Organization estimated that more than 1.9 billion adults worldwide are overweight and of these over 600 million were obese. This accounts for nearly 40% of adults worldwide!

Being overweight is a major risk factor for a number of chronic diseases, including diabetes, cardiovascular diseases, and cancer. Once considered a problem only in high-income countries, obesity is now dramatically on the rise in low- and middle-income countries, particularly in urban settings.

Overweight and obese are defined as abnormal or excessive fat accumulation that presents a risk to health. A crude measure of obesity in popular use is the Body Mass Index (BMI), which is defined as a person’s weight (in kilograms) divided by the square of his or her height (in metres). A person with a BMI of 30 or more is generally considered obese. A person with a BMI equal to or more than 25 is considered overweight.

WHY DO SOME OF US SEEM TO PUT ON WEIGHT MORE EASILY THAN OTHERS?

There is growing evidence that weight gain and obesity are the result of a complex interaction between our environment (i.e. our diet and lifestyle) and our genetics.

In terms of environment, the recent high availability of certain types of energy-dense foods as well as a decrease in physical activity due to the increasingly sedentary nature of many forms of work has led to a significant increase in obesity over the past 30 years. In terms of genetics, susceptibility towards weight gain in some individuals means that (for a significant portion of us) this inactivity and ready access to certain foods has led to serious health issues.

DO I HAVE A GENETIC PREDISPOSITION TO PUT ON WEIGHT?

Among the obesity-susceptibility genes recently identified in scientific studies, there is one gene in particular that has been observed to have a particularly strong association: the FTO gene. There are two possible gene variants that you can carry at this position in your DNA: a T allele or an A allele. As we all carry two copies of every gene (one from Mum and one from Dad) this means there are three possible ‘genotypes’: AA, AT, or TT.

Just how much difference does it make? Well, if you carry just one A allele, you are 1.3 times more likely to be obese than someone with the TT genotype, whereas if you carry two A alleles you are over 1.6 times more likely to be obese! In one meta-analysis on over 38,000 people, the 16% of people with the AA genotype weighed 3kg more and had 1.67 times increased odds of obesity versus those without the risk allele.

It also seems to be quite pervasive in different populations: the A risk allele has been associated with obesity in multiple different backgrounds, including Caucasian, African American, Mexican, Japanese, Scandinavian, and Han Chinese.

THE ‘A’ RISK ALLELE Interestingly, the effect of the FTO gene variant does not appear to be metabolic in nature, but instead has a role in appetite regulation through changes in the levels of certain chemical messages that tell our bodies how hungry or full we feel.

Studies have consistently shown that carriers of the A allele tend to feel hungrier, consume more food, and show a preference for high-fat foods over non-carriers. In short, they are genetically programmed to have a different brain response to food.

While the precise mechanism is still to be determined, we do know that the FTO protein itself produced by the FTO gene is expressed 1.5-times more in AA-genotype people than TT-genotype people following a period of fasting, and is highly expressed in the hypothalamus. In addition, the same study found AA individuals exhibited a 2.5-times increase in the hormone ghrelin, often termed the ‘hunger hormone’ in the media.

THE ‘HUNGER HORMONES’: HOW APPETITE WORKS

What exactly is it that makes us feel hungry? Biologically speaking, it can be attributed to fluctuating levels of two hormones: ghrelin and leptin.

Ghrelin, informally known as the ‘hunger hormone’, increases appetite. It is released primarily in the stomach and signals hunger to the brain. Research has suggested that ghrelin levels play a large role in determining how quickly hunger comes back after we eat. The quicker your ghrelin levels rise, the sooner you feel hungry again after a meal.

Leptin by contrast is the ‘satiety hormone’ and its presence makes you feel full. It is produced by fat cells and suppresses your appetite. In general, the more fat you consume, the more leptin is in your blood. Unfortunately for many obese people, they develop resistance to to the appetite-suppressing effects of leptin, so even with higher circulating levels, they don’t feel the effects.

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