Obesity is not simply about eating a lot more than you expend and becoming fat from the excess energy stored as fat; it’s a far more subtle interaction between genetics and environment. But in the case of obesity, the exact genes that are responsible for bringing about the condition are dispersed and hard to spot. Thankfully, every year scientists get newer insights into the genetics behind obesity and the environmental factors that may trigger these genes.
One such environmental exposure would be chemicals including pesticides, and one researcher conducted an experiment to determine whether dichlorodiphenyltrichloroethane (DDT) had such an effect. Much to his surprise, DDT increased the probability of developing obesity, but this occurred several generations after the first exposure.
DDT is a chemical that was first synthesized in 1873, but gained prominence at the onset of World War I, where it was used to control typhus and malaria. After the war, it became widely used in America as a pesticide with potent effect. It wasn’t until 1962 that its potential harm was highlighted by Rachel Carson’s Silent Spring, and in 1972, it was banned from usage in the US. It is however used in small quantities in some parts of the world.
It is described by America’s Environmental Protection Agency as PBT pollutant; Persistent, Bioaccumulative and Toxic. This means that it remains in the environment for a long time (15 years) before it can degrade, and even then, it breaks into still harmful compounds. It accumulates in animals that consume contaminated substances.
Mice are Exposed to DDT
In the experiment that sought to determine whether exposure to DDT could cause obesity, the researchers took pregnant mice (generation F0) and exposed them to DDT, while keeping every other thing normal. Another batch of mice remained unexposed to DDT, and was the control group.
Unrelated littermates of the subsequent F1 generation were then bred and the F2 generation they bore bred to bring about the F4 generation of mice. This breeding included mating unexposed mice to exposed mice.
These mice were later euthanized and genitourinary tissues taken for analysis.
Histological and Genetic Exams
The dissection enabled the researchers to vividly see among which generations abdominal adiposity had increased, and the histological samples were analyzed for disease conditions often associated with obesity.
The samples were also taken through several arrays to check out for genetic transformations.
The F1 generation strongly exhibited the symptoms associated with DDT exposure, such as kidney and ovarian disease, but obesity did not manifest itself prominently.
Obesity was manifested in the F3 generation, as more than half of the mice became obese, even though they were kept and nourished in conditions similar to previous generations.
The genetic basis for this oddity was uncovered by tests that revealed germline mutations in the F3 generation. The mutation was not a change in the genetic structure per se, but an alteration of how the genes are switched on or off, which alters the sequences of synthesized proteins and this disrupts normal physiological functions.
What is The Significance of All This?
Treating a condition requires one to understand the etiology of the condition, which is why anti-malarial medication would not work on a person suffering rabies. Once scientists have understood all the variables that can bring about obesity, tackling it becomes much easier.
There are studies that have suggested that the genetic drivers behind childhood obesity differ from those of adult obesity, and an understanding of this will help medical professionals to come up with better combined therapies that will tackle obesity and its attendant troubles effectively.
It also stresses the importance of avoiding such exposures, because while it may not harm you, your descendants could come to suffer.