As reported by the American Heart Association (2006), almost 70% of the total population of the United States has cardiovascular disease. As shown in the charts in the paper (Health Care Online, 2011), males are more prone to develop CVD than women at the age below 60. Men die 10 years younger than women from heart attacks (Kannel et al., 1976). However, this biological advantage of women over men shrinks as they age. The primary biological advantage of women over men in terms of CVD risk is the female sex hormone, estrogen. Estrogen protects women from cardiovascular disease. Most of the protective functions of estrogen originate from its role in controlling cholesterol levels. This hormone works in the liver to eliminate unnecessary cholesterol in the body (Saleh Connell, 2007). More particularly, estrogen boosts the level of good cholesterol and high-density lipoprotein (HDL) and minimizes the buildup of bad cholesterol or low-density lipoprotein (LDL). Bad cholesterol buildup blocks blood vessels which then can disrupt blood flow to the heart. In contrast, good cholesterol reduces these blockages by minimizing the level of bad cholesterol (Vitale, Miceli, Rosano, 2007). Estrogen strengthens the prostacyclin receptor. The prostacyclin receptor, which soothes the production of vascular smooth muscle cells and minimizes pulmonary vascular disorders, is a primary goal for estrogen being controlled by the estrogen receptor proteins— ERa and ERb (Saleh Connell, 2007). Prostacyclin receptor can hinder the tightening of vessel walls, blood clotting, and clustering of platelets (Sugden, 2001). Thus the protein can help protect the body from heart disease. Estrogen also prevents the development of dangerous blockages by working on white blood cells. These white blood cells can cause blockages by accumulating in the interiors of blood vessels (Sugden, 2001). Women in their childbearing years have a higher amount of protein annexin-A1 in their white blood cells compared to men. Annexin-A1 stops white blood cells from aggregating in the blood vessel wall which can cause vascular disorder (Sugden, 2001). Therefore, Pre-menopausal women are less prone to CVD than post-menopausal ones. Epidemiological studies reported lower CVD risk factors among estrogen-enriched women. These findings resulted in the assumption that estrogen-enhancing therapy, such as the use of birth control pills and hormone replacement therapy (HRT), for a specified period of time before the onset of the menopause is feasible. It is assumed that estrogens assume a major physiological function when the heart exhibits reperfusion disorder, which is an injury to the renal blood vessels (Saleh Connell, 2007). Normally, estrogen activity is interceded by particular estrogen receptors (ERs). ERs are part of the primary group of steroid hormone receptor, which can function as endothelial nitric oxide synthase (eNOS), which serves a vital function in sustaining vascular homeostasis by combining and discharging a number of soothing elements, like prostacyclin (Saleh Connell, 2007), with possible repercussions for coronary heart function. Nevertheless, the use of birth control pills has been linked to the raised amount of C-reactive protein related to CVD. This C-reactive protein (CRP) is generated in the body as a reaction to inflammation (Mendelsohn, 2002).

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