Gender-Based Differences in Cardiovascular Disease - Literature review Example

?Running Head: Biology Gender-Based Differences in Cardiovascular Disease (CVD) I. Introduction This paper discusses gender-based differences in cardiovascular disease. According to the World Health Organization (WHO, 2011), cardiovascular diseases (CVDs) are a set of blood vessel and heart disorders. Mostly, CVD is caused by the accumulation of extra plaque on the outer layer of a large blood—this is also referred to as ‘atherosclerosis’. This excess plaque disrupts the flow of blood to the brain or to the heart which causes heart attacks (Eaker et al., 1993). 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 above (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. II. Biological Theories 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 higher amount of the 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). Recurrently high CRP levels have been connected to CVD, and inflammation is assumed to contribute in the hardening and tightening of the arteries. According to some findings, use of birth control pills and HRT increases the risk of inflammation and levels of CRP (Mendelsohn, 2002). These findings indicate that estrogen may also promote CVD in postmenopausal women who use estrogen-enhancing therapies. Experts say that the likelihood of developing heart disease due to contraceptive use is further increased for heavy smokers. III. Psychological Theories Sex-based disparities in CVD risk are partially biologically oriented and partially psychologically or socially explained. In spite of years of study, CVD’s underlying pathophysiology is still quite complicated and as weakly verified as the social or psychological mechanisms involved in its treatment, identification, and symptoms. Three of the most studied psychological factors that increase CVD risk for men and post-menopausal women are Type A behavior, smoking, and poor diet. Type A Behavior Type A coronary prone behavior is currently regarded as one of the major psychological risk factors for CVD in women and men. Type A coronary-prone behavior is typified by lack of sympathy, competitiveness, and aggressiveness (Schaubroeck, Ganster, & Kemmerer, 1994). Helgeson (1990) emphasizes that stereotypical maleness, which is normally characterized by the Type A behavior, enhances the likelihood of CVD for men. Helgeson (1990) elaborates that there are economic and cultural factors linked to the development of this type A coronary-prone behavior in men. These are discussed below. Numerous researchers have reported that gender differences in CVD are brought about by sex-based disparities in role stereotypes. One reason in which ‘being a male’ may be connected to CVD is through health stereotypes. The male health stereotype discourages men from recognizing weaknesses and from seeking support when they feel they may require it. It is even likely that socialization has trained males not to entertain symptoms and emotions that they view as weaknesses (Link & Phelan, 1995). Hence, men have displayed more failures to comply with common health standards, communicate their symptoms, and consult healthcare professionals in comparison to women (Helgeson, 1990). Moreover, as stated in the article of Helgeson (1990), close relationships among men usually are limited by competitiveness, masculinity, and homophobia. These aspects of female-male relationships have a tendency to undermine the level of intimate openness and trust. Perpetuation of the conventional male gender stereotype has been linked to lack of openness and homophobia (Helgeson, 1990). Masculinity is also related with lack of empathy, a vital social ability exercised to sustain a healthy social support system. Studies putting emphasis on the capacity to interact and sympathize with others have demonstrated that males are not as capable as women in these domains (Helgeson, 1990). Smoking Smoking is the cause of more fatalities from CVD than any other illnesses and stands for one of the primary gained risk factor for CVD. Smokers are highly prone to blood clots, which consequently bring about severe circulation disorders. They also have increased risk for artery congestions, which are a steady accumulation of fat deposits. These congestions and clots cause acute CVD. Cigarette smoking is directly related to ischemic CVD, atherosclerosis, and acute coronary thrombosis (Link & Phelan, 1995). Particularly, in younger females, in which the frequency of cigarette smoking is presently elevating, smoking is evidently the major risk factor for unexpected death from heart attack. That smoking reinforces the possibility of thrombosis, or the development of a blood clot in the blood vessel’s interior, is indicated as well by the direct link between myocardial infarction, or simply known as heart attack, and cigarette smoking in comparison to a less direct link with angina pectoris (Link & Phelan, 1995). Thus, smokers are more prone to heart attacks than non-smokers. Males were discovered to be four times more likely to develop a myocardial infarction compared to premenopausal females (Sugden, 2001). Nevertheless, according to Vitale and colleagues (2007), even though the prevalence of myocardial infarction is normally higher among males, the prevalence in female chain smokers surpassed that of male non-smokers. Diet Poor diet can increase the likelihood of CVD for men than in pre-menopausal women. The connection between CVD and diet has usually placed emphasis on fat consumption and its effect on cholesterol levels and blood triglycerides (Link & Phelan, 1995). Medical findings have showed that risk factors for CVD normally are aggregates of hypertension, diabetes mellitus, obesity, and dyslipidemia. Poor diet among men and women increases the levels of cholesterol, saturated fat, and trans fat that can cause heart diseases (Link & Phelan, 1995). High levels of cholesterol, saturated fat, and trans fat, heighten the risk of CVD for men and for postmenopausal women. The connection between high levels of cholesterol and heart diseases are already discussed in the previous section. A poor diet normally comprises excess saturated fat. Just like cholesterol, saturated fact builds up in arterial walls, clogs them and raises blood pressure, resulting in stroke or heart attack (Link & Phelan, 1995). Another usual part of a poor diet is trans fat, which raises the levels of bad cholesterol and low-density lipoprotein, reduces high-density lipoproteins and good cholesterol (Vitale et al., 2007). It is assumed that the relationship between estrogen and other female sex hormones and specific contributing factors for metabolic disorder contributes to the gender disparity in CVD. Excessive weight and inactive lifestyle, according to Schaubroeck and associates (1994), are significant risk factors for CVD in post-menopausal women than in men. Metabolic disorder is reduced by estrogen levels. Hence, one crucial concern majority of post-menopausal women who have diabetes is the effect of estrogen replacement treatment on the occurrence of disorder in metabolism. IV. Critique The discussion shows that major biological determinants of cardiovascular disease intermingle with social or psychological factors throughout the developmental life cycle to affect vulnerability to illness. Women have a lesser tendency to develop cardiovascular disorder than men, as explained in the preceding discussion. This is due partly to gender-based biological processes, like the presence of estrogen, which have a defensive cardiovascular function, but also to sex-based disparities in vulnerability to, and acquired coping with and managing of, external stressors. The current discovery that women are genetically more diverse than men contributes much to the understanding of why particular illnesses, like cardiovascular disease, are discovered in diverse occurrences in women and men. But it is the contention of this paper that gender-based differences in CVD can be controlled since those are not wholly biologically determined. For instance, even though the CVD mortality rate of women is lower than that of men by 10 years, females encounter greater risk of severe effects and responses from cardiovascular disorder than males do. After a cardiovascular episode, women are more seriously weakened than men, endure more difficulties or complications, and have greater rate of mortality, particularly in the short term (Saleh & Connell, 2007). This is because of the conflicting and burdensome social demands and stereotypes women confront when experiencing infirmities. Nevertheless, as reported by McKinlay (1996), moving beyond individual characteristics, sex-based disparities in CVD diagnosis, treatment, and consequences are also brought about by gender discrimination in the provision of health care, government regulations, and accessibility health care. Hence, both external and internal environmental factors affect women’s and men’s CVD risk factors as they age. The risks generated by physical idleness, poor diet, and smoking for heart diseases can definitely be controlled by exercise, healthy diet, and regulated smoking. This paper acknowledges the intricate interaction between genetic, biological, psychosocial, and behavioral factors that influence health outcomes of individuals. Based on the biological and psychological theories discussed, this paper argues that individuals differ in their vulnerability to CVD and that these underlying disparities arise early in life. It argues that early environmental factors, biological, and genetic variables determine future psychosocial, behavioral, and economic directions that affect the manifestation of natural cardiovascular disease risk factors across genders. V. Summary Cardiovascular disease is uncommon in premenopausal women unless there is family history of lipid metabolism effects or cardiovascular disease. The occurrence of CVD in males is a number times higher than that of premenopausal females, yet these sex-based disparities decrease after menopause. Definitely, the risk for CVD is reinforced by the absence of estrogen, poor diet, physical inactivity, type A behavior, and heavy smoking. On the other hand, as determined by cardiovascular stimulation and stress hormones, women are more frequently vulnerable to continued levels of psychophysiological stress than men are. Constant stress can weaken health through deterioration of the body, like disrupting the arteries’ tissue lining, which increases CVD risk factors. Severe stress can also induce blood clots that can stimulate cardiovascular episodes. More studies are required to determine and verify whether gender-based disparities in CVD risk factors and response to stressors contribute to the understanding of gender differences in health disease exposure, diagnosis, treatment, and outcome in general. References n.a. (2006). Heart Disease Statistics, http://www.cardio360.com/heart-disease-statistics.html Eaker, E., Chesebro, J., Sacks, F., Wenger, N., Whisnant, J., & Winston, M. 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