Iron Increases Heart Disease


Iron Increases Heart Disease Essay, Research Paper

Coronary Artery Disease (CAD) has afflicted man throughout history. Diet and hereditary factors obviously are the key components in developing this condition. Foods high in cholesterol and saturated fats are often implicated in hastening or aggravating heart disease. Many disease states such as diabetes mellitus and hypertension have also been shown to increase a persons chances for CAD. Heart disease usually affects persons over age 60, but can be seen in people who are much younger for various reasons. This disease remains the number one cause of hospitalization and death in the adult population in western society (McCance and Huether, 1994).

The purpose of this literature review is to investigate research dealing with the subject of increased serum iron levels and the prevalence of CAD. Medical journals were primarily used for research data due to the nature of the subject and the need for in-depth analysis.

While it has the highest prevalence of any disease, women experience only 30-50% of the coronary artery disease incidence and mortality of age-matched men (Meyers, 1996). Many feel that this may be due to the protective effect that estrogen has on the blood vessels of females. There may actually be a direct correlation to reduced serum iron levels due to menses. Whereas men ” build-up” iron in the blood, women cleanse themselves of iron buildup on the monthly basis. Meyers (1996) also states that oxidation, the process in which an atom increases its positive charges (Miller and Keane, 1992), of low density lipoprotein cholesterol is important in atherosclerosis, and since oxidation is catalyzed by iron, it has been hypothesized that the lower iron stores of women reduce their risk of CAD through lessened lipid peroxide, a by-product of oxidation.

Numerous studies have been conducted to actually see if a relationship between serum iron or serum transferrin, (serum iron concentration divided by total iron-binding capacity), and heart disease or myocardial infarction, (heart attacks) exists. Sempos and Looker, (1994) used a total of 4518 men and women to conduct the first study of its kind on the subject of iron and CAD. Frequent serum iron levels, collected from 1971-74, and followed up through 1987, showed the risk of CAD was not related to serum transferrin levels in white men or women. Indeed, an inverse association of total body iron stores and overall mortality was shown, that is moderate to high serum transferrin associated with lower mortality.

In a similar study, 6086 men and 6102 women, who were randomly chosen, were followed for 14 years having frequent serum iron and total iron binding capacity (TIBC) levels drawn. Total Iron Binding Capacity refers to the amount of red bloods cells that are actively bound with iron at any given time. At the end of the study, 739 men and 245 women died from coronary artery disease. It was concluded that there was no relationship between TIBC and coronary mortality observed in men. In women, an inverse although not statistically significant association was found (Reunanen et al, 1995).

Sullivan (1996) states that the iron hypothesis, which hypothesizes increased serum iron causes CAD, provides a conceptual tool for study of the mechanisms by which age and gender influence the development of ischemic heart disease. The assumption that age and gender exert unalterable effects has diverted attention from these strong risk factors, and has led to intense preoccupation with weaker risk factors such as cholesterol. Which as he states, “has become a rigid and institutional point of view to determine CAD risk”.

High iron may indirectly cause damage to coronary arteries due to increased oxidation. Hauenschild et al, (1997) report that the association between nutrition and coronary heart disease is mainly due to the effect of nutrients on serum lipoproteins, the form in which fats are transported in the blood (Miller and Keane, 1992). Cholesterol intake does not play a very important role for plasma cholesterol although there is a strong interindividual difference in response. Low iron intake leads to an accelerated uptake of low-density lipoprotein into the macrophage. In another interesting study, Fields and Lewis, (1997), investigated low iron levels in rats and the incidence of CAD. They found that reduction of iron intake reduced blood levels of both triglycerides and cholesterol in rats fed a copper deficient diet containing fructose. They hypothesized that the combination of high iron, low copper, and fructose may be responsible for increased levels of risk-factor metabolites associated with heart disease.

In regard to the above information, the research concludes that it is unlikely that high serum iron or transferrin is the direct cause of CAD. It may be likely though that having a high iron intake may indirectly effect the progression of heart disease by influencing oxidation of cholesterol and lipoproteins. No research concluded that the lower incidence of heart disease in women is based in-part by lower serum iron levels due to menses.

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