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Table 1 Role of maternal dietary components in the development of pre-eclampsia

From: Maternal nutritional risk factors for pre-eclampsia incidence: findings from a narrative scoping review

Pathophysiology of pre-eclampsia

Dietary components and mechanism

Poor placentation

Defective trophoblast invasion leading to reduced utero-placental blood flow and inflammatory response

Vitamin D

• Regulates inflammation in maternal uterine natural killer cells, which supports extravillous trophoblast invasion

• Regulates angiogenesis through stimulating VEGF

Vitamin B9 (folate) and B12

• Regulates homocysteine concentrations, which damages endothelial cells and increases trophoblast apoptosis

Oxidative stress

Vitamin C and E

• Important antioxidants that scavenges oxygen radicals in aqueous phase (C) and in cell membranes (E)

• Vitamin C involved in uptake of free iron in plasma

Essential trace elements

• Zinc, copper and selenium as components of important antioxidants (superoxide dismutase and glutathione peroxidase)

•Free iron and copper in plasma are pro-oxidative transition metals

Endothelial dysfunction and systemic inflammatory response

Omega 3 long-chain polyunsaturated fatty acids

• Regulates oxidative stress, inflammation and lowers triglyceride concentrations by reducing free fatty acid availability, increasing phospholipid synthesis and decreasing triglyceride-synthesizing enzyme activity

• Increased concentration of circulating lipids accumulate in endothelial cells, which decreases release of prostacyclin (an endothelium-derived vasodilator) and results in endothelial dysfunction

Maternal syndrome with clinical signs of pre-eclampsia


Healthy dietary patterns

• Maternal metabolic or insulin resistance syndromes associated with endothelial dysfunction or sensitivity

• Diets characterized by high consumption of fruits, vegetables and whole grains, fish and seafood high in omega-3 fatty acids, monounsaturated vegetable oils, and low in added sugar are protective against cardiovascular diseases and metabolic syndromes

High blood pressure

Vitamin D and calcium

• Low serum calcium triggers increased secretion of parathyroid hormone (PTH), which stimulates release calcium stores from bone reservoirs, opens calcium channels to increase intracellular calcium, which leads to vasoconstriction and high blood pressure

• PTH stimulates calcitriol production and calcitriol increases calcium absorption from the intestine

• PTH activates the renin–angiotensin–aldosterone signalling pathway, which increases the vascular volume though sodium and water reabsorption