973-953-5500 / 1-833-512-1245

Lacking a sweet tooth could be genetic — and it could hold the key to fighting obesity.

In 2013, the American Medical Association formally added obesity to its list of diseases. But long before the condition was recognized as an illness, the world’s pharmaceutical companies have been searching for a cure.

Obesity is often attributed to simple science: eat too much and exercise too little, and you’re bound to gain weight. But newer research suggests that a gene variant may be to blame for the millions of Americans who tend to pack on the pounds. Just as there is a seemingly genetic predisposition to obesity, researchers have found a genetic predisposition to avoiding obesity. It’s a rare genetic mutation called essential fructosuria and only 1 in 300,000 people are carriers.

Skinny “genes”

As humans, we’re unable to make fructose — a natural sugar found in fruits, vegetables and honey — on our own. We acquire it from various foods and drinks. Consuming too much is associated with obesity, type 2 diabetes and liver ailments like fatty liver disease.

People with essential fructosuria tend to have an aversion to sweets. They lack the primary enzyme needed to metabolize fructose, so it is excreted in their urine. As a result of their genetics, they’re less likely to develop obesity and other related health issues.

Because the anomaly is so uncommon, health researchers stumbled upon it by chance. Pharmaceutical giant Pfizer, the largest U.S. drug maker, has been unable to track down a single carrier of the mutation in its quest to develop new treatments for obesity. Despite its rarity, researchers are eager to study essential fructosuria. The mutation could uncover new drug options for people struggling with the disease.

The fructose connection

The University of Denver has pioneered the idea of curbing fructose metabolism to prevent disease.  Scientist Richard Johnson discovered that mice without the fructokinase enzyme had lower blood glucose and insulin levels and gained less excess weight compared to those with the enzyme, while eating a high-fructose diet.  

Johnson’s discovery was confirmed by two University of California at Davis scientists, Kimber Stanhope and Peter Havel. Their research, published in the Journal of Clinical Investigation, showed that fructose was associated with weight gain and increased the risk factors of metabolic syndrome in humans. These findings were pivotal in changing the way many scientists looked at fructose and its connection to problematic health issues.

The simplest way to fight obesity  

Researchers believe that the essential fructosuria anomaly could have a major clinical impact on the world’s obesity rates. But if you’re not a carrier and don’t want to wait for an effective treatment, abstaining from sugar can help combat the disease and its complications.