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Prenatal high-salt diet leads to complications in offspring

03/01/2019 // Michelle Simmons // Views

Tags: badfood, badhealth, blood vessels, cardiovascular disease, children's health, high blood pressure, high-salt diets, hypertension, pregnancy, salt, salty foods, sodium

A study finds that prenatal high-salt diets can cause cardiovascular disease in offspring. The study, which was published in the Journal of Hypertension, suggests that prenatal diets high in salt can increase oxidative stress and damage blood vessels in offspring.

• High-salt diet has been associated with hypertension, and prenatal high-salt diet increases the risk of cardiovascular diseases in the offspring.
• Researchers from China aimed to determine whether and how prenatal high-salt diet affects nitric oxide-mediated vasodilatation in the offspring.
• For the study, they fed pregnant rats with either normal-salt or high-salt diet.
• The results showed that a high-salt diet caused increases in the levels of oxidative stress markers in blood samples and mesenteric arteries in the offspring.
• The offsprings of mothers fed with high-salt diet also experienced reductions in antioxidant activity, serum superoxide dismutase, and catalase, as well as an increase in malondialdehyde.
• In the high-salt offspring, increased oxidative stress impaired renin-angiotensin system, which is a hormone system that regulates blood pressure and fluid balance.
• The study provides new information for understanding and early prevention of cardiovascular diseases in fetal origins.

In conclusion, the findings of the study suggest that prenatal high-salt diet damages nitric oxide-mediated vasodilatation by increasing oxidative stress, which also impairs the renin-angiotensin system.

To read more studies on the causes of heart disease, visit HeartDisease.news.

Journal Reference:

Liu Y, Qi L, Wu J, Xu T, Yang C, Chen X, Lv J, Xu Z. PRENATAL HIGH-SALT DIET IMPAIRED VASODILATATION WITH REPROGRAMMED RENIN-ANGIOTENSIN SYSTEM IN OFFSPRING RATS. Journal of Hypertension. December 2018; 36(12): 2369-2379. DOI: 10.1097/hjh.0000000000001865

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