A Western Diet May Adjust Epigenetic Marks on Children’s DNA and Damage The Nervous System

A recent study has shown that following a western diet even before your child is born may lead to dysfunction of his or her autonomic nervous system via epigenetic changes. A western diet is high in saturated fats, red meats, and empty carbohydrates while being low in fresh fruit and vegetables, whole grains, seafood and poultry. Eating this way has been linked to many diseases, including hypertension, heart disease, diabetes, and obesity. Now, research suggests epigenetics may be involved in the impact this diet has on the human body, particularly in males.

Clinical studies have revealed that there is a high risk of developing type II diabetes if autonomic dysfunction is present. Autonomic dysfunction is a condition in which the autonomic nervous system does not work properly, affecting the function of the heart, bladder, intestine, and blood vessels, among other organs. Some symptoms include dizziness and fainting, sweating abnormalities, digestive difficulties, and sexual problems.

In a study published in Cell Molecular Neurobiology, researchers found that mice exposed to a high-fat, high-sugar diet for a period of time before giving birth led to epigenetic modifications of their offspring’s compensatory renin-angiotensin system, RAS. The renin-angiotensin system is a hormone system that regulates blood pressure, fluid retention, and vascular resistance.

Renin, which is released primarily by the kidneys, stimulates the formation of angiotensin in blood and tissue, which in turn stimulates the release of aldosterone from the adrenal cortex. Therapeutic manipulations of this pathway are very important in treating hypertension and heart failure, diseases linked to the consumption of a western diet.

In this study, researchers exposed male and female mice to either a regular diet or a high-fat high-sucrose diet until mating. Pregnant females continued their particular diet until the pups were weaned on the 21^st day. After weaning, the offspring from both diet groups were fed a regular diet.

Several analyses were carried out using tissue samples of offspring, including DNA methylation bisulfite sequencing, real-time PCR (RT-PCR), and ACE2 specific activity assays. Exposure to this high-fat and high-sugar diet in gestating and nursing dams resulted in a reduction of ACE2 methylation in major organs such as the brain, kidney, and cecum (a pouch in the large intestine) in her children. Moreover, changes in gene expression of ACE2 and AT_1aR were also observed. The increase in gene expression ultimately translated into an increase in ACE2 activity.

ACE2 has been reported to play a critical role within the central nervous system in modulating autonomic function. Therefore, the increase in ACE2 activity is believed to alter autonomic function and, furthermore, potentially expose progeny to a higher sensitivity to cardiovascular and metabolic diseases.

The data from this study suggest that perinatal exposure to HFHSD resulted in epigenetic modifications of the compensatory brain RAS, potentially affecting plasticity of neuronal networks leading to autonomic dysfunction in the male offspring.

Recent studies suggest that epigenetic modifications, such as DNA methylation, play a critical role in the development of cardiovascular and metabolic diseases. This study demonstrates how a mother’s diet during pregnancy and prior to pregnancy may affect their offspring epigenetic modifications that can lead to the development of cardiovascular and metabolic diseases in the offspring’s life.  The environment during pregnancy and early life is critical in shaping adults cardiovascular fitness and plasticity of the central nervous system. This suggests that we should consider the potential ramifications our diet may have not only on our own health but also on our children’s development.

Source: Mukerjee et al., Perinatal Exposure to Western Diet Programs Autonomic Dysfunction in the Male Offspring. Cell Molecular Neurobiology. 2018. 38, p.233-242.