Obesity During Pregnancy Increases the Risk of Lifelong Heart Disease in Offspring
Obesity is defined as an abnormal or excessive buildup of fat that poses a health risk. A BMI of 30 or above is considered obese.
Obesity has become increasingly prevalent in America. Recent estimates suggest that more than 42% of adults in the United States are obese. Health risks of obesity include type 2 diabetes, high blood pressure, heart disease, and sleep apnea. New research has found it might even have an impact on your children too.
According to a recent study, maternal obesity impacts the fetus’ heart health and function. The research, which was published in The Journal of Physiology, discovered that maternal obesity produces molecular changes in the fetus’s heart and modifies the expression of genes involved in nutrition metabolism, dramatically increasing the likelihood of cardiac problems in the child later in life.
Gene Expression Changes in the Fetus
This is the first study to demonstrate that the heart is ‘programmed’ by the nutrition it receives throughout birth. Gene expression changes affect how carbs and fats are metabolized in the heart. They change the heart’s nutritional preference away from sugar and toward fat. As a result, the hearts of obese female mice’s fetuses were bigger, heavier, had thicker walls, and displayed signs of inflammation. The heart’s ability to contract and circulate blood throughout the body is impaired as a result.
A mouse model that replicates human maternal physiology and placental nutrient transfer in obese women was used by researchers from the University of Colorado, US. Female mice (n=31) were given a high-fat diet along with a sugary drink, which is roughly equal to a person eating a burger, chips, and a soft drink on a daily basis (1500kcal). Female mice were fed this diet until they became obese, gaining roughly 25% of their initial body weight. A control diet was fed to 50 female mice.
Mouse pups (n=187) were studied in utero, as well as after birth at 3, 6, 9, and 24 months using imaging techniques, including echocardiography and positron emission tomography (PET) scans. Researchers analyzed the genes, proteins, and mitochondria of the offspring.
Sex-Specific Differences in Offspring Cardiac Health
The changes in offspring cardiac metabolism strongly depended on sex. The expression of 841 genes was altered in the hearts of female fetuses and 764 genes were altered in male fetuses, but less than 10% of genes were commonly altered in both sexes. Interestingly, although both male and female offspring from mothers with obesity had impaired cardiac function, there were differences in the progression between sexes; males were impaired from the start, whereas females’ cardiac function got progressively worse with age.
The sex difference in the lasting impairments of cardiovascular health and function could be due to estrogen. Higher levels in young females may protect cardiovascular health, the protection diminishes as estrogen levels deplete as the females age. The molecular cause for the sex difference is not yet understood.
Lead author, Dr. Owen Vaughan, University of Colorado, US said:
“Our research indicates a mechanism linking maternal obesity with cardiometabolic illness in the next generation. This is important because obesity is increasing rapidly in the human population and affects almost one-third of women of childbearing age. By improving our understanding of the mechanisms involved, this research paves the way for treatments that could be used in early life to prevent later-life cardiometabolic illnesses, which are costly for health services and affect many people’s quality of life. For example, we could offer more tailored advice on nutrition to mothers or children based on their body mass index or sex, or develop new drugs that target metabolism in the heart of the fetus.”
Mice have shorter pregnancies, more offspring, and different diets than humans so further studies on human volunteers would be required to extrapolate the findings to women’s health. Loss-of-function studies also need to be carried out to prove this mechanism linking maternal obesity and offspring heart function and pinpoint the exact molecules responsible.
Reference: “Maternal obesity causes fetal cardiac hypertrophy and alters adult offspring myocardial metabolism in mice” by Owen R. Vaughan, Fredrick J. Rosario, Jeannie Chan, Laura A. Cox, Veronique Ferchaud-Roucher, Karin A. Zemski-Berry, Jane E. B. Reusch, Amy C. Keller, Theresa L. Powell and Thomas Jansson, 11 May 2022, The Journal of Physiology.
DOI: 10.1113/JP282462
Never miss a breakthrough: Join the SciTechDaily newsletter.
Follow us on Google and Google News.
1 Comment
Years ago I found a medical article online that concluded any kind of inflammation can cause the release of xanthine oxidase which then breaks down to uric acid and free radicals. Last year I found a medical article which explained that estrogen is protective against uric acid and post menopausal women not on hormone therapy are as likely to get gout as younger men. In humans, undiagnosed allergies to common foods and food additives (e.g. MSG, FDA approved for expanded use in 1980; obesity/diabetes epidemic presented by 1990, CDC/NCHS data) can still cause chronic low level inflammation. Assuming (as a lone lay investigator) the same is true for mice, current human statistics can support Dr. Vaughan’s findings after about two and a half generations of Americans unwittingly being exposed to metabolic manipulation in the form of undiagnosed allergies being aggravated to be more inflammatory by added ‘cultured’ MSG; heart disease officially being the leading cause of death in the US. Perhaps some kind of a professional clearing house of medical studies could ‘connect the dots’ like I do. Is anyone paying attention out there?