- Obesity is a risk factor for several of the leading causes of premature and preventable death.
- One fifth of children in the United States are considered obese.
- New research in mice has shown that environmental and nutritional changes during pregnancy and early development can cause epigenetic changes in the area of the brain related to food intake, activity and metabolism in mice.
- The work also highlights similar links between the human and mouse genomes, suggesting that similar epigenetic changes may also occur during human fetal development.
Obesity can seriously compromise a person’s physical and mental health. This definite as “abnormal or excessive fat accumulation that can impair health” and is a known risk factor for heart disease, type 2 diabetes, and certain types of cancer, all of which are leading causes of premature and preventable death.
Obesity rates have tripled since 1975, more 41% of adults and almost twenty% of children in the US are classified as obese. People are considered obese if they have excess body fat and a body mass index (BMI) greater than 30.
BMI is a simple but quite controversial measurement, defined as a person’s weight in kilograms divided by the square of their height in meters (kg/mtwo).
Recently, researchers at Baylor College of Medicine suggested that obesity risk in humans may be determined by environmental and genetic factors during early development and argue that obesity should be considered a neurodevelopmental disease.
study leader Dr. Robert A. Waterlandprofessor at Baylor College of Medicine, said Today’s medical news:
“[…] genetic variation certainly contributes to individual differences in body weight, environmental influences early in the development of body weight regulatory mechanisms (developmental programming) may, in general, play a larger role in determining individual propensity to obesity”.
The work published in the magazine Progress of science applications epigenetics to show that obesity is related to nutrition during certain phases of development.
A series of things such as poor diet, lack of physical exercise and lack of “Okay” sleep, are known to increase risk of obesity
The type and quantity of food eaten are also directly related to the risk of obesity; consuming too many calories and burning too few will create a calorie surplus that will lead to weight gain. That said, the public health message to eat less and exercise more hasn’t stemmed the tide of obesity.
Once viewed as a result of a lack of will and self-control, the biological nature of obesity has been shown to be much more complex. In fact, prenatal and early life studies have linked malnutrition to obesity in rats.
The effect of nutrition during early development on human studies has shown that famine during the first trimester of pregnancy resulted in higher rates of obesity, but famine during the last trimester and first few months of life was associated with lower levels of obesity.
is widely accepted that body weight is also influenced by genetics. the Centers for Disease Control and Prevention reports on 50 different genes that have been associated with obesity. Genes determine the signals that hormones transmit to the brain, where they direct the body to eat or move.
Large-scale human genome studies have found changes in BMI-related genes that are expressed in the developing brain.
Epigenetics studies the way genes work, which allows scientists to study how behavior and the environment can alter how genes work. Epigenetic changes do not change the DNA sequence, they change the way the body reads the DNA sequence.
For this study, mice from 2 to 4 months of age were monitored during pregnancy and their pups were studied during postnatal development.
Whole genome analysis and RNA sequencing were completed on neuron Y glial cells and studied epigenetic markers and gene expression. Specifically, the researchers used tissue from the arcuate core of the brain’s hypothalamus, the area that controls hunger and satiety.
The researchers noted that the postnatal period in mice is critical for obesity-related epigenetic changes and regulation of energy balance, suggesting that obesity could be a “consequence of dysregulated epigenetic maturation,” according to Dr. Harry MacKay. , first author of the study.
Interestingly, when comparing the epigenetic data with data from human genome studies, the researchers found a strong correlation between regions of the human genome related to BMI and areas of epigenetic changes in mice, suggesting that adult obesity may be determined in part by epigenetic development in the arcuate nucleus.
The authors propose that this new understanding may create “effective interventions to prevent obesity.” This work provides the argument that early prenatal and postnatal development may, at least in part, determine human obesity risk.
“[E]Evidence from the last few decades indicates that once a person is obese, it is extremely difficult to achieve a “normal” body weight. And, when obese adults lose a significant amount of weight, it is extremely difficult to maintain long-term weight loss. We hope that a better understanding of the developmental neuroepigenetic mechanisms underlying the establishment of body weight regulation will enable effective approaches to prevent obesity.”
— Robert A. Waterland, MD
When asked if the work could lead to new nutritional recommendations for pregnancy, Dr. Waterland commented that the current research, which was done in mice, “does not provide a basis for making nutritional recommendations for humans. Although we don’t have the data yet, it’s a reasonable assumption that the postnatal epigenetic maturation we cataloged in this mouse study occurs during late fetal development in humans.”
“[…] Such data would reinforce existing recommendations that women aim to achieve a healthy body weight before becoming pregnant, as maternal obesity during pregnancy not only increases the risk of pregnancy complications such as preterm birth and gestational diabetes, but also appears to promote a lifelong positive energy balance in her developing child,” he added.
The study is not without limitations.
The constantly changing nature of the cell population during early development makes interpretation of the data complicated, it is possible that changes in the cell population between time points could affect the results.
The authors plan to overcome this in future studies by using more time points and using computational models.
The next step for the research is to extend it to human studies.
“[…] An obvious next step is to determine when this BMI-associated epigenetic maturation occurs in humans. Because many neurodevelopmental processes occur earlier in humans than in mice, it is likely that this hypothalamic epigenetic maturation occurs during late fetal development in humans,” Dr. Waterland said.
“[A]The obvious next step would be to try to determine whether maternal obesity during pregnancy somehow affects these developmental changes, resulting in persistently poor regulation of energy balance in her child.”
— Robert A. Waterland, MD
