Epidemiological observations have long suggested a role for nutritional deficiencies (i.e., calcium, proteins, vitamins, etc.) in pre-eclampsia. However, intervention evaluations have failed to confirm such promising observations. We will describe here the evidence from randomized controlled trials that supports the relationship between different nutrients and pre-eclampsia.
There is considerable evidence linking calcium intake and hypertension during pregnancy from observational and experimental studies. However, there is still no satisfactory explanation for the mechanisms involved in the calcium-mediated effect on blood pressure reduction. It has been postulated that parathyroid hormone could be involved in this relationship. Demonstrated alterations in extracellular calcium homeostasis in pre-eclampsia include hypocalciuria and decreased serum levels of calcitriol. Increased parathyroid hormone (PTH) and decreased plasma ionized calcium concentration have not been consistently observed. Also, consistent abnormalities of intracellular calcium metabolism have been described in pre-eclamptic women, such as increased intracellular free calcium concentration in platelets and lymphocytes. Increases in intra-cellular free calcium concentration in circulating cells are hypothesized to result from fluctuation in hormones or vasoactive substances that cause similar alteration in vascular smooth muscle. Pregnancy is a state of high calcium requirements as a result of fetal demands while maternal adaptive mechanisms are partially inhibited. These phenomena lead to the hyper-parathyroid state of pregnancy. An increase of parathyroid hormone serum levels would involve an increase of free intracellular calcium. Then, the concentration of intracellular free calcium in vascular smooth muscle cells determines the degree of tension, and is the trigger for muscular contraction. So the vasoconstrictive effect, with a rise in blood pressure, results from an increase in vascular smooth muscle tension.
An additional role for nutrition in the genesis of pre-eclampsia could be nutritional factors that strengthen oxidative stress, leading to pre-eclampsia. A nutritional factor could be the deficiency of antioxidant intake, specifically vitamin C and E. Vitamin C is central for the neutralization of both water-soluble and lipid-soluble free radicals; as a water-soluble molecule its ability to neutralize free radicals in the aqueous compartment is clear. Also, ascorbate is not made in humans and must come from diet. Vitamin E, a potent antioxidant, has been suggested to play a role in preventing pre-eclampsia.
Nutritional factors other than antioxidants can also contribute to oxidative stress. Hyper-homocysteinemia can occur as a result of dietary deficiencies. Hyper-homocysteinemia as a risk factor for pre-eclampsia is said to be altered, at least in part, by the genesis of oxidative stress. Vitamin B6 and B12 and folic acid are involved at different steps in the metabolic pathway for removing or recycling homocysteine to methionine. Dietary deficiencies of any of these micronutrients can increase circulating homocysteine. Pre-eclampsia is characterized by increased triglycerides that favor the formation of small, dense low-density lipoproteins (LDLs). This lipoprotein variant has increased access to the subendothelial space where it is sequestered from blood-borne antioxidants. The relevant role of triglycerides in the genesis of pre-eclampsia is indicated by the fact that they are increased long before clinically evident disease. Similarly, free fatty acids are increased in pre-eclampsia and this increment can be observed months before the diagnosis. Recent studies indicate that this effect may be secondary to altered copper binding by albumin to which large amounts of free fatty acids are bound. Unbound copper is a potent stimulator of free radical formation. Ordinarily this effect of copper is prevented by protein binding (quantitatively, primarily to albumin). However, with fatty acid binding, albumin binds copper differently. In this configuration, copper bound to albumin maintains its ability to participate in redox reactions. Thus, it appears that increased free fatty acids can also contribute to oxidative stress.
All of these nutritional alterations may be amenable to dietary modification raising the possibility of nutritional prophylaxis.
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