The Expression of Obesity Genes: A Comprehensive Impact on Appetite and Fat Breakdown

3.1.2 Expression of obesity genes

Congenital obesity is definitely a genetic disease, determined by multiple genes, either because the relevant genes are expressed or their expression is suppressed. People who are prone to obesity later in life may be "susceptible" and their obesity is also controlled by genes, with the relevant genes being expressed insufficiently or excessively. Obesity in other normal people is caused by normal acquired "environmental" factors.

(1) Obesity genes increase appetite

How do obesity genes play a role in the process of obesity in humans?

Some obesity genes, such as the "FTO" gene, increase calorie intake. Scientists conducted an experiment on 2,726 children aged 4 to 10 in Scotland. The children were given the freedom to choose from a variety of foods at each meal, including sausages, cheese, bagels, various fruits and vegetables, and water. The results showed that children with the FTO gene mutation preferred high-fat, fried foods and sweets, consuming an average of 100 more calories per meal.

In other words, "FTO" alters people's eating patterns. Furthermore, dopamine is a neurotransmitter in the brain, primarily responsible for transmitting feelings of excitement and pleasure. Studies have found that obese individuals have fewer dopamine receptor genes compared to underweight individuals, meaning they need to eat more food to experience pleasure.

(2) Obesity genes make it difficult for fat to break down.

Some obesity genes can inhibit the body's energy expenditure. Researchers, after comparing the weight of two groups of Mexican Americans, found that the group with more active CRTC3 genes was more obese. This is because the expression of genes like CRTC3 slows down fat burning, thus leading to obesity.

Studies have found that obese individuals exhibit various DNA abnormalities. Some DNA sequences inhibit normal insulin secretion, while others suppress the formation of chemicals essential for insulin synthesis. Furthermore, β3-adrenergic receptors (β3-AR) are distributed in human abdominal fat cells, and research shows that individuals with β3-AR gene mutations have a lower basal metabolic rate than non-mutant individuals. Among obese individuals, the number of those carrying β3-AR gene mutations is higher than that of non-mutant individuals, meaning that obese individuals have lower energy expenditure for basic life activities.

Children who are obese have a higher number of fat cells and are more prone to obesity in adulthood; but why do many people who were not obese as children become obese as adults? American scientists recently discovered a gene called GIRK4, which is related to regulating food intake and energy expenditure. Disruption of the normal function of this gene is a potential cause of obesity in adults aged 20 to 60.

More than 200 genes or chromosomal regions associated with obesity have been discovered to date.

(3) The activation of obesity genes begins in the fetal period.

Genes are inherited, but environmental factors can alter the strength of genes!

The most typical example is the Pima Indian tribe in the United States. Their lives used to be extremely impoverished. After entering modern society, their lives improved dramatically. As a result, more than 95% of the Pima Indians became obese.

Furthermore, the number of obese children is surging because junk food is cheap, high in calories, and readily available, tempting a large number of individuals with the FTO gene mutation. Studies have confirmed that the FTO gene is present in childhood, which is related to "children's overeating."

The genes for obesity are activated as early as the fetal stage. One mother, fearing her fetus would be malnourished, desperately tried to supplement her diet, resulting in the birth of a 13-pound baby who remained obese throughout infancy, childhood, and adolescence.

Why is this? Scientists have discovered that higher levels of body fat in mothers before and during pregnancy promote the release of beta cells, which in turn affects the fetal hypothalamus's metabolic processes related to weight control. Studies have found that obese infants have a higher number and size of fat cells than normal-sized infants.

(4) Excessive stress can also activate obesity genes.

German researchers conducted a survey of over-indebted individuals in Germany between 2006 and 2007 and found that 25% of them were obese, compared to only 11% in the general population.

British researchers conducted a 19-year study on working professionals and found that "people with high work stress have a 73% higher rate of obesity compared to those who have never experienced high work stress."

Why does stress cause weight gain?

Stress activates obesity genes. Some obesity genes increase appetite, and when people are in stressful situations (such as facing financial problems or pressure from their boss), it ignites their passion for carbohydrate-rich foods. Only when these foods are eaten will stress hormones decrease.

Stress can increase fat storage. For our prehistoric ancestors, stress meant natural disasters or the approach of wild animals. The body needed extra energy to cope with food shortages or fight off wild animals, so the process of rapidly storing fat was very important.

Malnutrition places a tremendous strain on the body. Studies have found that if pregnant women experience malnutrition in the early to mid-stages of pregnancy, their children have a 50% chance of becoming obese in adulthood. This is because humans evolved in environments of food scarcity, developing conservation genes. These genes enhance digestion, increase energy absorption, and reduce energy expenditure, thereby promoting fat synthesis. It is currently believed that malnutrition during the embryonic or infant stages leads to an upregulation of conservation gene expression, causing more stem cells to differentiate into fat cells.

Sleep deprivation also puts stress on the body. A study by French scientists showed that if a person sleeps an average of only 4 hours for two consecutive days, the level of ghrelin, the hormone responsible for hunger, will nearly double, while the level of leptin, the hormone that regulates body fat and appetite, will relatively decrease.