Obesity and sedentary behaviors are commonly viewed as a reflection of cultures with widespread availability of cheap high-calorie and high-fat foods, often in developed countries like the U.S. Behavioral patterns of overeating are often viewed as a conscious choice, but research has found that consistent food choices may lead to hard-wired obesity predisposition, particularly through prenatal and early life exposure to high-fat and high-calorie diets. Obesity may be a series of poor choices that lead to permanent brain changes that impact not only the obese individual but also the development and fate of their children. Perhaps not only you, but also your children, are what you eat.
Over-nutrition in prenatal and early life diets has been found to cause brain abnormalities that predispose children to obesity and development of cognitive and memory impairments. Numerous studies using mice models have revealed alarming impacts from high-fat diets both in utero and during the weaning (nursing) period. Pregnant female mice on high-fat diets during pregnancy and weaning resulted in offspring that were hyper-insulemic and hyper-leptinemic. Offspring were also heavier at birth and remained heavier during the weaning period.
High-fat diets increase resistance to leptin, an important hormone involved in sending signals to the brain to stop eating. Leptin acts on receptors in the hypothalamus to inhibit hunger signals. Leptin resistance impairs food-reward-related brain signaling, so individuals have a higher food intake threshold they need to reach in order to feel satisfied. The hypothalamus is the area of the brain involved in hunger drives. Excessive feeding in early life leads to hypothalamic dysfunction, which intensifies eating drive into adulthood, resulting in weight gain. Insulin is a hormone that allows your body to use glucose from food to provide energy for cells. High-fat diets lead to insulin resistance, predisposing children to early development of type II diabetes.
High-fat diets can also induce local pro-apoptotic (cell death) signaling in the hippocampus. Reduced hippocampal size in obesity may accelerate later life cognitive impairment and potentially increase the risk of developing neurodegenerative diseases such as Alzheimer’s disease. The hippocampus is an area of the brain vital for cognition, learning, processing of short to long term memory, spatial navigation, as well as emotions. A poorly developed or damaged hippocampus results in a reduction in executive functioning and attention, decreasing global functioning and lower IQ.
Impacts of Maternal and Paternal Obesity on Childhood Brain development
Maternal obesity during pregnancy reduces production of hippocampal BDNF, an important regulator of neuronal development survival, memory and cognitive ability; it also suppresses food intake. BDNF levels are reduced by inflammatory cytokines. Production of inflammatory cytokines is increased in obese individuals, leading to impaired hippocampal function by decreasing levels of important regulators like BDNF. Genetic obesity is also linked to reduced hippocampal BDNF expression and increased cytokine expression and hippocampal inflammation.
There are also paternal connections to obesity predisposition. A mice study revealed fathers who were obese at the time of conception can pass on obesity predisposition to their children and the next generation. Obese male mice were mated with normal diet and normal weight females. Analysis of microRNAs in the sperm of the obese fathers revealed that high-fat diet changes the molecular makeup of sperm, which program embryos for increased risk of obesity.
What does this mean?
Essentially, when children’s brains develop in an environment of excess nutrition, the brain needs that same level of nutrition to feel satisfied. High-fat diets during prenatal and postnatal development as well as genetic influences from the mother and father have drastic effects on a child’s ability to eat properly and function normally. The brain may be hard-wired for high-fat diets, increasing the likelihood of developing obesity. Obesity not only affects physical functioning, but has stark impacts on cognitive abilities as well. Children exposed to high-fat diets may have reductions in executive functioning and attention, decreased global functioning and lower IQ’s.
What can we do?
Unfortunately, prenatal and early life over-nutrition is an issue that cannot be solved simply by telling people to eat healthier. Accessibility to healthy food varies due to factors such as socioeconomic status. Foods high in fat, salt, and preservatives are cheaper than fruits and vegetables, and those of lower SES face the dilemma of letting their family go hungry or feeding them unhealthy food. As research in the realm of obesity continues, a greater call to action is needed to change the food system by which our country is built around, which is no easy task. But how long are we willing to sacrifice the bodies and brains of our children before we make a change?
Sources:
Female mice research article: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2671057/
Male mice research article:
http://www.eurekalert.org/pub_releases/2013-07/foas-odp071113.php
You Are What You Eat: Early Life Diet and Obesity Risk
