There are definitely some genes that can cause obesity. Though some of us may have the genes that predispose us to obesity and type 2 diabetes, predisposition does not mean pre-destiny.
If you have a family history of obesity or type 2 diabetes, or you are of Asian, East Indian, Native American, Pacific Islander or Middle Eastern heritage, you are much more likely to be carbohydrate intolerant. A little bit of sugar or starch will cause you to make way more insulin than others. This starts you on the vicious cycle of weight gain, hunger, and fatigue. The good news is that by eating well and exercising you can completely prevent obesity and type 2 diabetes.
There are other genes that play a role in weight gain and weight loss as well.
The brain has genes that code receptors for dopamine, the pleasure producing neurotransmitter. Some of these genes cause the dopamine receptors to be less responsive to the pleasure signals provided by dopamine. Many drugs of abuse, including cocaine and heroin, trigger dopamine receptors.
The abundant abuse of drugs that are available freely and over the counter also triggers these dopamine receptors. These drugs are commonly known as “sugar” and “refined carbs”!
When your dopamine receptors need more stimulation to feel pleasure, it predisposes you to cravings and addiction. We know that sugar acts just like cocaine and drives food addiction and causes overeating. Some people have mutations or SNPs on their dopamine genes which will increase their risk for addiction. We report on these genes in the Nervous System DNA report.
Other genetic factors also play a role. Just as different people have varying responses to carbs, they also have different responses to fats. This is new and emerging research, and more is being discovered every day. Some people do better with more omega-3 fats, while some do better with saturated fats, and still others do better with more omega-6 fats. Different people need different levels for balance. There can be a big difference in how your body responds to different fats and how they affect your blood sugar, cholesterol, and even gut bacteria. What we do know for sure is that having mutations on the PGC1A gene will mean that we may be less likely to metabolise fats well (oh no Keto is not great)!
Variations in genes involved in the regulation of food intake, FTO (fat mass and obesity-associated gene); leptin, the leptin receptor (LEPR); and ghrelin, may contribute to obesity risk by reducing satiety and increasing hunger.
Leptin is the ‘satiety hormone’ which inhibits hunger and stimulates metabolism after eating and during physical activity. It is opposed by ghrelin, the ‘hunger hormone’, which generates the desire to eat when energy levels are low. In obesity, leptin levels are higher and ‘resistance’ (loss of sensitivity) to leptin may occur, so one never feels full.
Variances on the LEPR gene can also reduce sensitivity to leptin, having the same effect of reducing satiety and increasing the likelihood of overeating and obesity. The FTO gene is associated with predisposition to obesity due to its role in control of food intake and food choice. Variances on FTO confer a preference for energy-dense foods, higher fat intake and bigger meal size due to down-regulated adipocyte (fat cell) production of leptin.
Nutrition and lifestyle is interventions can dramatically reduce our risks. Our genes are not our destiny!
