Sunday, June 24, 2012

Gene Obesity

According to the World Health Organisation (WHO) the prevalence of overweight or obese people has tripled since 1980. Over 65% of people in the U.S. and over 50% of people in the U.K. were overweight or obese in 2010. Alarmingly the number of overweight children is also increasing.

The massive change in our eating habits is now leading to obesity linked diseases of epidemic proportions. But is it all down to society and poor eating habits? Research has shown that there appears to be another cause, or at least another contributory factor.

Our DNA may hold the key. When you consider how complicated new life is to create on a molecular level it's no wonder that sometimes there are mutations in DNA. If the mutation allows you to successfully reproduce and pass on the mutated DNA then the possibility of passing on future disease is immense.

A number of mutations have been identified that are thought to contribute to obesity. Research is continuing and the mechanisms involved are poorly understood in some cases. But the mutations discovered so far generally appear to affect the part of the brain (hypothalamus) that deals with appetite rather than metabolism.


Leptin is a hormone that is produced by the cells that store fat. The amount of Leptin circulating in the blood is directly proportional to the amount of fat stored by your body. It signals the part of your brain that controls appetite and causes appetite to be suppressed.

A mutation has been found in the Leptin gene and also to the protein (receptor) that locks Leptin on to the brain cells. If Leptin or its receptor is prevented from functioning properly because of the mutation then the brain does not receive the appetite suppression signals and you keep eating.

Fat Mass and Obesity-Associated Protein (FTO)

Fat mass and obesity-associated protein (FTO) is an enzyme. It is thought to be involved with the breakdown of fats and the repair of DNA. It has been found to be present in the hypothalamus in the brain.

A mutation to the gene that synthesises FTO can increase the amount of FTO released into your system. Increased FTO levels have been seen to induce overeating and increased fat storage. This mutation has been linked to type II diabetes.

Brain-derived Neurotrophic Factor (BDNF)

BDNF is a growth factor that is involved with the growth and survival of nerve cells. If less BDNF is synthesised by its mutated gene then the feeling of satisfaction after a meal is reduced, causing you to continue eating.

Insulin Induced Gene 2 (INSIG2)

INSIG2 is a protein that blocks the production of cholesterol. If less INSIG2 is available then more cholesterol is produced.

Cholesterol is transported in blood by proteins forming low density lipoproteins (LDL) or high density lipoproteins (HDL). Too much cholesterol in the blood can lead to heart and artery disease.

Niemann-Pick Disease Type C1 (NPC1)

NPC1 is a protein that helps to transport cholesterol within cells. A known mutation causes cholesterol to become trapped. This leads to accumulation of cholesterol inside the cell which is unable to escape.

Since your system can't access the cholesterol it is forced to produce more some of which also becomes trapped inside the cells.

Mutations of the NPC1 gene have been linked to weight gain. Research has shown that it may be associated with appetite control.

There are many more known mutations that are thought to be associated with weight gain and obesity. Since the effects of the weight gain do not prevent reproduction these mutated genes have being passed down through the generations. Perhaps it is only now that these mutations are widespread enough to be noticed.

Although these gene mutations make it easier to over eat it is possible to control the amount you consume. It may require a vast amount of willpower and a good deal of knowledge about food but with guidance it may be possible to restore healthy eating and a balanced diet.

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