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Abuse as a Gendered Risk Factor for Cardiovascular Disease: A Conceptual Model

Scott-Storey, Kelly A. RN, MN, PhD(c)

The Journal of Cardiovascular Nursing: November/December 2013 - Volume 28 - Issue 6 - p E1–E8
doi: 10.1097/JCN.0b013e318279e372

Background: Cardiovascular disease (CVD) is one of the most serious health challenges facing women today. Investigations into CVD risk factors specific to women have focused primarily on sex-based differences, with little attention paid to gender-based influences. Abuse, such as child abuse, intimate partner violence, and sexual assault, is a serious gendered issue affecting one quarter to one-half of all women within their lifetime. Despite beginning evidence that abuse may increase CVD risk in women, the biological, behavioral, and psychological pathways linking abuse to CVD have received little attention from researchers and clinicians.

Purpose: The aim of this study was to propose a conceptual model that delineates the pathways by which abuse may increase CVD risk among women. Within the model, lifetime abuse is positioned as a chronic stressor affecting CVD risk through direct and indirect pathways. Directly, abuse experiences can cause long-term biophysical changes within the body, which increase the risk of CVD. Indirectly, smoking and overeating, known CVD risk behaviors, are common coping strategies in response to abuse. In addition, women with abuse histories frequently report depressive symptoms, which can persist for years after the abusive experience. Depressive symptoms are a known predictor of CVD and can potentiate CVD risk behaviors. Therefore, depressive symptoms are proposed as a mediator between lifetime abuse and CVD as well as between lifetime abuse and CVD risk behaviors.

Conclusions and Clinical Implications: To better promote cardiovascular health among women and direct appropriate interventions, nurses need to understand the complex web by which abuse may increase the risk for CVD. In addition, nurses need to not only pay attention to an abuse history and symptoms of depression for women presenting with CVD symptoms but also address CVD risk among women with abusive histories.

Kelly A. Scott-Storey, RN, MN, PhD(c) Lecturer, Faculty of Nursing, University of New Brunswick, Fredericton, Canada.

The author has received a Regional Partnership Program Doctoral Research Award (2009–2012) funded by the Canadian Institutes of Health Research, the New Brunswick Health Research Foundation, and the University of New Brunswick.

The author has no conflicts of interest to disclose.

Correspondence Kelly A. Scott-Storey, RN, MN, PhD(c), Faculty of Nursing, University of New Brunswick, PO Box 4400, Fredericton, NB, Canada E3B 5A3 (

Cardiovascular disease (CVD) is one of the most serious health challenges facing women today.1,2 According to the World Health Organization,3 CVD is the single leading cause of mortality among women, accounting for one-third of all deaths worldwide; similarly, in the United States and Canada, CVD accounts for 1 of every 3 deaths.4,5 For approximately 38 million women in the United States and 1.3 million women in Canada, CVD is a chronic and often debilitating disease.6,7 Empirical evidence suggests that women not only live longer than men with CVD but also have worse prognoses and spend approximately twice as many years disabled as measured by loss of productivity, functional limitations, and emotional distress.1,6,8

However, women’s health remains a relatively new area of interest within the cardiovascular arena; only within the past few decades have women been purposefully included in large cardiovascular research initiatives.9,10 These efforts have identified important sex-based biological and physiological differences between men and women (eg, differences in the size of coronary arteries; the role of estrogen in CVD) that have better informed the prevention, assessment, diagnosis, and treatment of CVD among women.6,11,12 Despite medical advances, mortality from CVD is not decreasing as rapidly among women as among men for reasons that remain largely unknown.2 One explanation may be that we have failed to take into account the contextual gendered aspects of a woman’s life that affects health.

Gender refers to the “array of socially constructed roles, attitudes, personality traits, behaviors, values, and relative power and influence that society ascribes to two sexes on a differential basis.”13(p1) Evidence is rapidly accumulating to suggest that gender significantly influences health. For example, health risk behaviors such as cigarette smoking and physical inactivity are known to be different among men and women, primarily because of societal and cultural norms attributed to gender.12,13 Therefore, decontextualizing women’s health from gender-based influences greatly mitigates against identification of risk factors uniquely affecting women’s health.10 One proposed gendered risk factor that may influence the cardiovascular health of women is abuse.

The purpose of this article was to put forward a conceptual model derived from empirical and theoretical knowledge that delineates how lifetime abuse (current and/or past) may increase the risk for CVD among women (Figure). Within this model, lifetime abuse is positioned as a chronic stressor directly increasing the risk of CVD through physiological changes within the body.14–16 Common coping strategies for dealing with stress from abuse, such as smoking and overeating, are known CVD risk behaviors.14,17 These CVD risk factors are an indirect pathway by which lifetime abuse can affect CVD. In addition, women with abuse histories have higher rates of depressive symptoms.18,19 Depression is associated with CVD and can also potentiate the adoption of CVD risk behaviors.14,20–22 Therefore, depressive symptoms are proposed to mediate the effect of lifetime abuse on CVD as well as the CVD risk behaviors of smoking and overeating. A better understanding of the complex pathways by which abuse may increase CVD risk is an important step in reducing the burden of this disease among vulnerable groups of women.



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Cardiovascular Disease

Cardiovascular disease is a broad term that refers to any disease involving the cardiovascular system and is caused by the interaction of genetics, health risk behaviors, and environment.4 Besides being a leading cause of death and disability among women,3 it is estimated that CVD costs the Canadian economy more than $22 billion annually in physician services, drug costs, hospital costs, disability, and lost productivity.7 In 2008, in the United States, an estimated $298 billion was spent on CVD-related healthcare costs; this is in comparison with $228 billion spent for all cancers combined.5

Despite significant reductions in CVD mortality in most developed countries between 1980 and 2000, recent trends in CVD risk factors are worrisome, especially among younger age groups.23 Decreases in smoking rates have slowed, whereas rates of obesity, diabetes, and hypertension are on the rise, translating into a projected new increase in the incidence of CVD, especially among young women.23–26 Prevention therefore becomes paramount in reducing the economic impact and in improving the health of women. Unfortunately, established risk factors (ie, smoking, physical inactivity, improper nutrition, general stress, overweight/obesity, high blood pressure, and diabetes) explain only a portion of the incidence and prevalence of CVD.27 To reduce the burden further, additional risk factors need to be identified and investigated; gender-specific risk factors for women, such as abuse offer a critical new field for exploration.

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Lifetime Abuse

Abuse as a Gendered Risk Factor

Abusea against women is globally recognized as a gendered issue and a major public health problem affecting one quarter to one-half of all women within their lifetime.28–30 It is a universal phenomenon affecting women regardless of ethnicity, age, socioeconomic status, level of education, or religion.31 Abuse is defined as the “intentional use of physical force or power, threatened or actual, against another person that either results in or has a high likelihood of resulting in injury, death, psychological harm, maldevelopment or deprivation”32(p4) Abuse against women is inextricably linked to gender-based inequalities perpetuated by religious, ethnic, cultural, societal, and political norms that uphold women’s subordinate status in society, ultimately creating power inequality between men and women.33,34 This power imbalance has led to the domination and discrimination of women by men through physical, psychological, and sexual abuse; rape; sexual exploitation; sexual harassment; trafficking; and prostitution, thereby validating abuse as a pervasive gendered issue greatly affecting women.33,35 Although men are also victims of abuse, the overall incidence is lower in comparison with women, and women continue to bear the brunt of more serious forms of abuse.36,37

Abuse can manifest in various types throughout the lifecycle, including child sexual, physical, and/or psychological abuse; child physical and emotional neglect; adult sexual assault; and intimate partner violence. It is an unfortunate reality that those who experience abuse are frequently the victims of multiple types of abuse (eg, physical, sexual, and psychological) that often co-occur and reoccur across the lifespan, resulting in a cumulative abuse profile.38 These cumulative experiences of abuse are believed to compound over time, leading to incrementally worse health outcomes, highlighting the importance of examining abuse across the lifespan.38 For example, Fogarty and colleagues39 demonstrated a “super-additive risk” of depressive symptoms for women exposed to abuse in both childhood and adulthood compared to women who experienced abuse at only 1 of the time points.

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Abuse and Cardiovascular Disease

Abuse is associated with a wide array of adverse health outcomes40,41; however, research examining the relationship between abuse and CVD is relatively new. In seminal works, Dong42 provided evidence of a link between childhood trauma (inclusive of abuse) (n = 17 337) and heart disease in adulthood, reporting a 30% to 70% (dose response relation) greater risk of heart disease among those with childhood trauma(s). Using data from the National Comorbidity Study (n = 5308), Batten and colleagues43 found that women with abuse histories had a 9-fold increase in CVD compared with women with no abuse history and researchers using US national survey data (n = 70 156) discovered that women with a history of intimate partner violence were almost twice as likely to report CVD as women with no such history.44 Despite identified associations between abuse and CVD, elucidating the causal pathways by which abuse may increase CVD risk has been limited. One emerging pathway receiving attention is chronic stress. And although stress itself is not a “new” risk factor in the development and progression of CVD, the identification of abuse as a chronic stressor increasing the risk is a fresh perspective within cardiovascular research.

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Abuse and Chronic Stress

Abuse is a significant stressor that often results in persistent and chronic stress, regardless of whether the abuse exposure is current or in the past.14 In other words, stress continues long after the abuse stops. Any single experience of abuse can produce chronic stress; however, women often experience cumulative abuse across the lifespan, leading to greater stress and augmented health risk.38 Furthermore, for women who have experienced abuse, a multitude of factors commonly coexist that continue to generate stress, such as fear, lack of control, isolation, conflict with family and friends, poor health, changes in economic status, ongoing harassment, and abuse.45–47

When a stressor is encountered, a powerful physiological response involving the cardiovascular, immune, neuroendocrine, and nervous systems is initiated.16 Activation of these systems during times of acute, short-term stress is adaptive as it promotes the survival and well-being of the individual.15 However, in situations where stress is persistent, as is often the case with abuse, chronic activation of the stress response becomes maladaptive, producing significant and long-term neuroendocrine, metabolic, haemostatic, immunologic, and inflammatory changes within the body.16 This compromised state is known as allostatic load (or overload), which leads to vulnerability for disease development, such as CVD.15

The physiological mechanisms at play in situations of chronic stress that increase the risk for CVD are complex and interrelated. For example, according to the works of McEwen and Lasley15 and Sapolsky,48 chronic stress can lead to the dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, the primary structure in the brain responsible for maintaining physiologic balance in the face of stress (ie, homeostasis and allostasis). The result is a prolonged release of stress hormones, such as cortisol and epinephrine, which causes the heart to beat more rapidly, produce more efficient contractions, and increases blood pressure as a means to promote greater blood flow and delivery of oxygen and glucose to vital muscles and organs required in the stress response. Chronic or frequent cardiovascular stimulation via this mechanism can result in hypertension. Hypertension in turn reduces the external diameter of blood vessels through a process known as “vascular remodeling,” leading to even greater resistance in vascular blood flow and perpetuating the hypertensive state.49 Chronic hypertension has numerous damaging effects on the cardiovascular system, including, but not limited to, left ventricular hypertrophy, congestive heart failure, and even kidney failure.49,50 In addition, high levels of circulating cortisol as a result of chronic stress leads to the suppression of the immune system.15 Immune suppression results in a low-grade chronic inflammatory state, which leads to endothelial damage of blood vessels and the development/progression of atherosclerosis, a major contributor to CVD.15,51,52 The presence of a chronic inflammatory state has been supported by studies demonstrating an association between past abuse and higher physiological markers of inflammation.53,54 For a detailed review on the physiologic changes associated with abuse and stress, see Keeshin et al,55 Black and Garbutt,51 or Out et al.54

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Cardiovascular Disease Risk Behaviors

Abuse also affects health indirectly through health risk behaviors. Women use a range of behaviors to cope with the stress radiating from the abuse (current or past).14,42 Some behaviors, such as smoking and overeating, which are common among women with abuse histories, unfortunately increase the risk for CVD. For example, Scott-Storey and colleagues17 found that within a community sample (n = 309), women with abusive histories were 3 times more likely to be current smokers compared with the national population average (44.1% vs 15.5%, respectively). Similarly, Dichter et al56 reported that among a sample of 21 162 women, the odds of smoking were 3 times higher for women reporting intimate partner violence.

Cigarette smoking is one of the most significant modifiable risk factors for the development of CVD,4,25 with smokers being 2 to 4 times more likely than nonsmokers to develop the disease.57 Inhaling the mixture of chemicals in tobacco smoke increases CVD risk through a number of biological pathways, including the promotion of thrombosis formation, platelet aggregation, chronic inflammation, lipid abnormalities, and endothelial damage; also, it increases circulating levels of catecholamines and fibrinogen and increases myocardial workload.58

Women with abuse histories are at greater risk for being overweight/obese, likely in part related to stress.40 In a population-based survey, adult women who reported a history of child sexual or physical abuse had approximately twice the likelihood of being obese compared with women with no such history.59 In a sample of more than 11 000 California women, researchers discovered that those who were overweight were 32% more likely to report that they had been abused as children compared with women of normal weight.60

Stress is believed to influence the development of overweight/obesity through adverse changes in eating behaviors.61 Although stress can suppress appetite, approximately 70% of individuals will increase their food intake (overeating) during times of stress, particularly of high-fat, carbohydrate-dense foods.62 This type of behavior is referred to as “emotional” or “comfort” eating because it serves as both a coping mechanism and a mood stimulant but unfortunately leads to adverse weight gain.61 In addition, depression is associated with decreased energy and engagement in less physical activity, thereby contributing to adverse weight gain.14,63 In turn, overweight and obesity are independent risk factors for CVD, being associated with left ventricular hypertrophy, hypertension, cardiomyopathy, ischemic heart disease, atherosclerosis, dyslipidemia, metabolic syndrome, heart failure, and atrial fibrillation.64–66 Moreover, stress can influence the development of overweight and obesity through more direct biophysical mechanisms. For instance, unremitting stress results in chronic hyperactivity of the HPA axis, leading to sustained cortisol production.15 The result of prolonged cortisol exposure is weight gain, especially visceral/abdominal fat accumulation, which is a particularly potent risk factor for CVD.66 Furthermore, the excess adipose tissue itself expresses proinflammatory molecules, which in turn potentiates the inflammatory state underlying CVD processes such as atherosclerosis.65

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Depressive Symptoms

The final pathway through which abuse can affect CVD is through depression. Depression is characterized by feelings of intense sadness or depressed mood, as well as some combination of feelings of hopelessness, guilt, worthlessness, changes in appetite, sleep disturbances, loss of interest, irritability, lack of energy, and difficulties in concentration.67 Evidence suggests that both clinical depression and subclinical depressive symptoms (symptoms that do not meet the diagnostic criteria threshold for clinical depression but that still significantly impact the well-being of the individual) are associated with increased morbidity and mortality.68

Researchers have demonstrated both prospectively and retrospectively that women who have experienced any type of abuse across the lifespan are at a greater risk for clinical depression and subclinical depressive symptoms when compared with those with no such history.18,69 For example, in her meta-analysis, Golding19 found that the odds of depression occurring in women with a history of intimate partner abuse were approximately 4 times greater than that of women with no abusive history. Recently, Dichter et al56 reported similar results, finding the odds of having depression to be nearly 4 times greater for those women with a history of intimate partner violence (n = 21 162). Furthermore, childhood sexual and physical abuse has been associated with doubling the odds of depression in adulthood, speaking to the long-lasting effects of abuse.59

A multitude of complex cognitive, social, behavioral, psychological, and biological mechanisms are at play, increasing vulnerability to depression among those with a history of abuse.14,40 Focusing solely on biology, depression may partially be the consequence of physiological abuse-related changes in brain structures (eg, corpus collosum, hippocampus, amygdala) and the HPA axis, which ultimately impacts behavior and mood.55,70 For instance, dysregulation of the HPA axis results in increased cortisol levels, which can lead to the breakdown of serotonin, an important neurotransmitter in the regulation of mood.40

Depression is often identified as an outcome of abuse; however, it may also influence the extent to which abuse adversely impacts a woman’s physical health, thereby positioning it as a mediator between abuse and physical health.14 Empirical evidence suggests that depression/depressive symptoms are associated with CVD. The results of 4 systematic reviews and meta-analyses indicate that in individuals with no known CVD, depression predicts the development of the disease, with a relative risk of 1.5 to 2.7, even after controlling for conventional risk factors.20–22,71 Although the precise physiological mechanisms are not well understood, depressed individuals both with and without established CVD have been shown to have chronically increased levels of cortisol, catecholamines, and inflammatory markers, all of which promote the development and progression of CVD.27,40,51

Depression may also foster CVD through engagement in health risk behaviors.14 It is well established that cigarette smoking is more prevalent among depressed individuals compared with nondepressed individuals, probably because it offers a way to cope with the negative emotions associated with depression.40,68,72 In a population-based survey of 3213 adults in the St Louis Epidemiologic Catchment Area study, individuals with a diagnosis of major depression had 2.9 times the odds of being a smoker compared with their nondepressed counterparts.73 Furthermore, depressed individuals with a history of abuse are more likely to smoke in comparison with depressed individuals with no such history, possibly representing an augmented effect of abuse on smoking behavior among depressed individuals.72

Depressive disorders and depressive symptoms are also positively associated with adverse weight gain.74,75 Results from a recent systematic review and meta-analysis of 9 prospective longitudinal studies showed that depressed individuals had a 58% increased risk of becoming obese with time.76 Furthermore, the severity of depressive symptoms seemingly has a linear relationship to weight, with greater depressive symptoms related to a faster rate of weight gain.77 It has been postulated that depression may lead to deleterious weight gain through changes in eating behavior, similar to what is seen in stress situations. Emotional or comfort eating is thought to function as a mood stimulant for many individuals and is more prevalent among individuals who are depressed or show depressive symptoms.75,78 As well, depression is characterized by long-term overactivity of the HPA axis and increased cortisol secretion.79–81 As mentioned previously, increased cortisol levels, in turn, have been positively associated with the development of obesity and specifically visceral obesity, a particularly potent CVD risk factor.66 This places depression as an important mediator of the relationship between experiences of abuse and overweight/obesity.

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The proposed conceptual model is an important contribution to women’s health as it addresses current gaps in our understanding of CVD by taking into account gendered influences such as abuse. This model provides a roadmap by which to understand the complex web of biological, psychological, and behavioral pathways increasing CVD risk among women who have experienced abuse. In particular, it suggests that lifetime abuse increases the risk of CVD through direct biological changes, as well as indirectly through CVD risk behaviors of smoking and overeating and depressive symptoms.

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Implications for Practice and Research

Nurses, in all aspects of their work, will encounter women who have experienced abuse. This model provides a guide for nurses to work with these women in the context of reducing the risk for CVD. Notably, the model highlights the link between lifetime abuse and CVD risk and underscores the importance of inquiring about abuse history in all women presenting with CVD risk factors, symptoms, and/or pathology. In light of the long-term cumulative effects of chronic stress on health, it is critical that nurses inquire about current and past abuse experiences.82 However, few nursing programs currently provide specific content on assessing and responding to abuse; therefore, training and institutional support to be able to appropriately respond to disclosures of abuse are necessary. Simply asking the questions without understanding the sensitive nature of the issue, nor having the capacity to offer support or access to resources, will mitigate efforts to reduce the impact of abuse on cardiovascular health.

A key message emerging from the model is the importance of a coordinated, multimodal approach to CVD risk reduction among women with abuse histories. Because of the intertwined connection among the physical, mental, and behavioral consequences of abuse, one cannot be adequately treated in isolation of the others, and without a multimodal approach targeted at both mental and physical health, efforts to reduce the risk of CVD will be attenuated at best. For example, the importance of assessing for and addressing depressive symptoms within the context of overall CVD risk reduction becomes clear as depression contributes not only to the pathophysiology of CVD but also to behavior and risk reduction adherence, particularly that of smoking cessation and weight management.83,84

Viewing abuse as a chronic stressor that is linked to risk behaviors provides a lens through which nurses can work with women. Traditional CVD lifestyle modification approaches that focus primarily on eliminating health risk behaviors such as smoking and unhealthy eating may not be appropriate for women who are coping with the stress of abuse. It is unsupportive and potentially harmful to condemn smoking or emotional eating without understanding the role that such behaviors play in the women’s life as a coping strategy. Rather, a harm reduction approach85 in which nurses work with women in identifying and reducing negative health behaviors while concurrently arming her with new healthy coping strategies might prove to be a more successful method. A harm reduction approach results in the formulation of individualized and realistic goals. Achievement of these goals may provide women, who have been in life situations where they feel powerless, with an opportunity to gain a sense that they have control over their life/body. The achievement of such goals, no matter how small they may be, improves not only the cardiovascular health of these women but also their mental well-being.

Positioning lifetime abuse as a gendered risk factor for CVD is a promising direction in our efforts to understand CVD among women. This model serves to direct research initiatives aimed at investigating women’s health, with the ultimate goal of being able to develop more effective health promotion and prevention strategies that improve cardiovascular health among women who have experienced abuse. Empirically testing the validity of the proposed model, as well as evaluating alternative models, will be the next step in understanding CVD risk among abused women.

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What’s New and Important

  • Abuse is identified as a potential gendered risk factor for the development of cardiovascular disease (CVD) amongwomen.
  • Amultivariable model is proposed by which abuse increases the risk for CVD through complex biological, behavioral, and psychological pathways.
  • Gendered sensitive thinking and research are needed to develop more effective health promotion and prevention strategies that reduce cardiovascular risk and ultimately improve cardiovascular health among women who have experienced abuse.
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The author thanks Dr Judy Wuest and Dr Marilyn Hodgins for their invaluable insight and mentorship.

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1. Heart and Stroke Foundation. Women and heart disease: the heart truth. Accessed February 12, 2012.
2. American Heart Association. Heart Disease Education, Analysis and Research, and Treatment for Women Act. Accessed June 12, 2012.
3. World Health Organization. The World Health Report 2004: Changing History. Geneva, Switzerland: World Health Organization; 2004.
4. Heart and Stroke Foundation. Statistics. Accessed May 2, 2012.
5. Roger V, Go A, Lloyd-Jones D, et al. Heart disease and stroke statistics—2012 update: a report from the American Heart Association. Circulation. 2012; 125 (1): e2–e220.
6. Mosca L, Banka C, Benjamin E, et al. Evidence-based guidelines for cardiovascular disease prevention in women: 2007 update. Circulation. 2007; 115 (11): 1481–1501.
7. Public Health Agency of Canada. 2009 tracking heart disease and stroke in Canada. Accessed July, 2012.
8. Mackay J, Mensah G. The Atlas of Heart Disease and Stroke. Geneva, Switzerland: World Health Organization; 2004.
9. Wenger N, Collins P. Women & Heart Disease. 2nd ed. Boca Raton, FL: Taylor & Francis; 2005.
10. Young L. Women’s health and cardiovascular care: a persistent divide. In: Morrow M, Hankivsky O, Varcoe C, eds. Women’s Health in Canada. Toronto, ON: University of Toronto Press; 2007: 456–476.
11. Bowles D. A radical idea: men and women are different. Cardiovasc Res. 2004; 61 (1): 5–6.
12. Pilote L. Sex-specific issues related to cardiovascular disease: a synopsis of the 2007 supplement. CMAJ. 2007; 176 (6): 789–791.
13. Health Canada. Sex and gender-based analysis (SGBA). Accessed May 2, 2012.
14. Schnurr P, Green B. Trauma and Health: Physical Health Consequences of Exposure to Extreme Stress. Washington, DC: American Psychological Association; 2004.
15. McEwen B, Lasley E. The End of Stress as We Know It. Washington, DC: Joseph Henry Press; 2002.
16. McEwen B. Central effects of stress hormones in health and disease: understanding the protective and damaging effects of stress and stress mediators. Eur J Pharmacol. 2008; 583 (2–3): 2–3.
17. Scott-Storey K, Wuest J, Ford-Gilboe M. Intimate partner violence and cardiovascular risk: is there a link? J Adv Nurs. 2009; 65 (10): 2186–2197.
18. Hegarty K. The relationship between abuse and depression. Nurs Clin North Am. 2011; 46 (4): 437–444.
19. Golding J. Intimate partner violence as a risk factor for mental disorders: a meta-analysis. J Fam Violence. 1999; 14 (2): 99–132.
20. Frasure-Smith N, Lesperance F. Depression and cardiac risk: present status and future directions. Heart. 2010; 96 (3): 173–176.
21. Rugulies R. Depression as a predictor for coronary heart disease: a review and meta-analysis. Am J Prev Med. 2002; 23 (1): 51–61.
22. Nicholson A, Kuper H, Hemingway H. Depression as an aetiologic and prognostic factor in coronary heart disease: a meta-analysis of 6362 events among 146 538 participants in 54 observational studies. Eur Heart J. 2006; 27 (23): 2763–2774.
23. Capewell S, O’Flaherty M. Trends in cardiovascular disease: are we winning the war? CMAJ. 2009; 180 (13): 1285–1286.
24. Lee DS, Chiu M, Manuel DG, et al. Trends in risk factors for cardiovascular disease in Canada: temporal, socio-demographic and geographic factors. CMAJ. 2009; 181 (3–4): 3–4.
25. Heart and Stroke Foundation. The Growing Burden of Heart Disease and Stroke in Canada. Ottawa, ON, Canada: Heart and Stroke Foundation of Canada; 2003.
26. Capewell S, Ford E, Croft J, Critchley J, Greenlund K, Labarthe D. Cardiovascular risk factor trends and potential for reducing coronary heart disease mortality in the United States of America. Bull World Health Organ. 2010; 88: 120–130.
27. Ford D. Depression, trauma, and cardiovascular health. In: Schnurr P, Green B, ed. Trauma and Health: Physical Health Consequences of Exposure to Extreme Stress. Washington, DC: American Psychological Association; 2004: 73–98
28. Statistics Canada. The Violence Against Women Survey. Ottawa, ON: The Daily; 1993.
29. Tjaden P, Thoennes N. Extent, Nature, and Consequences of Intimate Partner Violence : Findings From the National Violence Against Women Survey. Washington, DC: US Department of Justice, Office of Justice Programs, National Institute of Justice; 2000.
30. World Health Organization. Gender-based violence. Accessed May 2, 2012.
31. Roberts B. Violence against women: a risk factor for cardiovascular disease. Accessed May 2, 2012.
32. World Health Organization. World Report on Violence and Health. Geneva, Switzerland: World Health Organization; 2002.
33. Heise L. Violence Against Women: The Hidden Health Burden. Washington, DC: The World Bank; 1994.
34. World Health Organization. What is a gender-based approach to public health? Accessed July 12, 2012.
35. Kelly U, Gonzalez-Guarda R, Taylor J. Theories of intimate partner violence. In: Humphreys J, Campbell J, eds. Family Violence and Nursing Practice. New York, NY: Springer; 2011: 51–90.
36. Statistics Canada. Family Violence in Canada: A Statistical Profile. Ottawa, ON: Statistics Canada; 2011.
37. Rennison C. Intimate Partner Violence, 1993–2001: Bureau of Justice Statistics. Washington, DC: US Department of Justice; 2003.
38. Scott-Storey K. Cumulative abuse: do things add up? An evaluation of the conceptualization, operationalization, and methodological approaches in the study of the phenomenon of cumulative abuse. Trauma Violence Abuse. 2011; 12 (3): 135–150.
39. Fogarty C, Fredman L, Heeren T, Liebschutz J. Synergistic effects of child abuse and intimate partner violence on depressive symptoms in women. Prev Med. 2008; 46 (5): 463–469.
40. Kendall-Tackett K. Treating the Lifetime Health Effects of Childhood Victimization. Kingston, NJ: Civic Research Institute; 2003.
41. Plichta S. Intimate partner violence and physical health consequences. J Interpers Violence. 2004; 19 (11): 1296–1323.
42. Dong M. Insights into causal pathways for ischemic heart disease: adverse childhood experiences study. Circulation. 2004; 110 (13): 1761–1766.
43. Batten S, Aslan M, Maciejewski P, Mazure C. Childhood maltreatment as a risk factor for adult cardiovascular disease and depression. J Clin Psychiatry. 2004; 65 (2): 249–254.
44. Black M, Breiding M. Adverse health conditions and health risk behaviors associated with intimate partner violence—United States, 2005. Morb Mortal Wkly Rep. 2008; 57 (5): 113–117.
45. Ford-Gilboe M, Varcoe C, Wuest J, Merritt-Gray M. Intimate partner violence and nursing practice. In: Humphreys J, Campbell J, eds. Family Violence and Nursing Practice. New York, NY: Springer; 2011: 115–154.
46. Wuest J, Merritt-Gray M. Not going back: sustaining the separation in the process of leaving abusive relationships. Violence Against Women. 1999; 5 (2): 110–133
47. Wuest J, Ford-Gilboe M, Merritt-Gray M, Berman H. Intrusion: the central problem for family health promotion among children and single mothers after leaving an abusive partner. Qual Health Res. 2003; 13 (5): 597–622.
48. Sapolsky R. Why Zebras Don’t Get Ulcers: A Guide to Stress, Stress Related Diseases, and Coping. New York, NY: W.H. Freeman; 1994.
49. Larkin K. Stress and Hypertension Examining the Relation Between Psychological Stress and High Blood Pressure. New York, NY: Yale University Press; 2005.
50. Julius S. Sympathetic hyperactivity and coronary risk in hypertension. Hypertension. 1993; 21 (6): 886–893.
51. Black P, Garbutt L. Stress, inflammation and cardiovascular disease. J Psychosom Res. 2002; 52 (1): 1–23.
52. Brunner E. Stress mechanism in coronary heart disease. In: Stansfeld S, Marmot M, eds. Stress and the Heart: Psychosocial Pathways to Coronary Heart Disease. London, England: BMJ Books; 2002: 181–199.
53. Fernandez-Botran R, Miller J, Burns V, Newton T. Correlations among inflammatory markers in plasma, saliva and oral mucosal transudate in post-menopausal women with past intimate partner violence. Brain Behav Immun. 2011; 25 (2): 314–321.
54. Out D, Hall R, Granger D, Page G, Woods S. Assessing salivary C-reactive protein: longitudinal associations with systemic inflammation and cardiovascular disease risk in women exposed to intimate partner violence. Brain Behav Immun. 2012; 26 (4): 543–551.
55. Keeshin B, Cronholm P, Strawn J. Physiologic changes associated with violence and abuse exposure: an examination of related medical conditions. Trauma Violence Abuse. 2012; 13 (1): 41–56.
56. Dichter ME, Cerulli C, Bossarte RM. Intimate partner violence victimization among women veterans and associated heart health risks. Womens Health Issues. 2011; 21 (4): S190–S194.
57. Centre for Chronic Disease Prevention and Control. Heart disease and stroke. Accessed April 19, 2012.
58. US Department of Health and Human Services. The Health Consequences of Smoking: A Report From the Surgeon General. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Promotion, Office on Smoking and Health; 2004.
59. Rohde P, Ichikawa L, Simon G, et al. Associations of child sexual and physical abuse with obesity and depression in middle-aged women. Child Abuse Negl. 2008; 32 (9): 878–887.
60. Alvarez J, Pavao J, Baumrind N, Kimerling R. The relationship between child abuse and adult obesity among California women. Am J Prev Med. 2007; 33 (1): 28–33.
61. Wardle J, Gibson E. Impact of stress on diet: process and implications. In: Stansfeld S, Marmot M, eds. Stress and the Heart: Psychosocial Pathways to Coronary Artery Disease. London, England: BMJ Books; 2002: 124–149.
62. Adam T, Epel E. Stress, eating and the reward system. Physiol Behav. 2007; 91 (4): 449–458.
63. Public Health Agency of Canada. Women with heart disease: living a good life. Accessed October 1, 2012.
64. Malnick S, Knobler H. The medical complications of obesity. QJM. 2006; 99 (9): 565–579.
65. Ritchie S, Connell J. The link between abdominal obesity, metabolic syndrome and cardiovascular disease. Nutr Metab Cardiovasc Dis. 2007; 17 (4): 319–326.
66. Shively C, Register T, Clarkson T. Social stress, visceral obesity, and coronary artery atherosclerosis: product of a primate adaptation. Am J Primatol. 2009; 71 (9): 742–751.
67. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders: DSM-IV-TR. Washington, DC: American Psychiatric Association; 2000.
68. Katon W. Clinical and health services relationships between major depression, depressive symptoms, and general medical illness. Biol Pyschiatry. 2003; 54 (3): 216–226
69. Hedtke K, Ruggiero K, Fitzgerald M, et al. A longitudinal investigation of interpersonal violence in relation to mental health and substance use. J Consult Clin Psychol. 2008; 76 (4): 633–647.
70. Leeb R, Lewis T, Zolotor A. A review of physical and mental health consequences of child abuse and neglect and implications for practice. Am J Lifestyle Med. 2011; 5 (5): 454–468.
71. Wulsin L, Singal B. Do depressive symptoms increase the risk for the onset of coronary disease? A systematic quantitative review. Psychosom Med. 2003; 65 (2): 201–210.
72. Anda R, Croft J, Felitti V, et al. Adverse childhood experiences and smoking during adolescence and adulthood. JAMA. 1999; 282 (17): 1652–1658.
73. Glassman A, Helzer J, Covey L, et al. Smoking, smoking cessation, and major depression. JAMA. 1990; 264 (12): 1546–1549.
74. Blaine B. Does depression cause obesity? A meta-analysis of longitudinal studies of depression and weight control. J Health Psychol. 2008; 13 (8): 1190–1197.
75. Konttinen H, Silventoinen K, Haukkala A, Sarlio-Lahteenkorva S, Mannisto S. Emotional eating and physical activity self-efficacy as pathways in the association between depressive symptoms and adiposity indicators. Am J Clin Nutr. 2010; 92 (5): 1031–1039.
76. Luppino F, Penninx B, Zitman F, et al. Overweight, obesity, and depression: a systematic review and meta-analysis of longitudinal studies. Arch Gen Psychiatry. 2010; 67 (3): 220–229.
77. Needham B, Epel E, Adler N, Kiefe C. Trajectories of change in obesity and symptoms of depression: the CARDIA study. Am J Public Health. 2010; 100 (6): 1040–1046.
78. Canetti L, Bachar E, Berry E. Food and emotion. Behav Processes. 2002; 60 (2): 157–164.
79. Friedman M, McEwen B. Posttraumatic stress disorder, allostatic load, and medical illness. In: Schnurr P, Green B, eds. Trauma and Health: Physical Health Consequences of Exposure to Extreme Stress. Washington, DC: American Psychological Association; 2004: 157–188.
80. Marniemi J, Kronholm E, Aunola S, et al. Visceral fat and psychosocial stress in identical twins discordant for obesity. J Intern Med. 2002; 251 (1): 35–43.
81. Nemeroff C. The corticotropin-releasing factor (CRF) hypothesis of depression: new findings and new directions. Mol Psychiatry. 1996; 1 (4): 336–342.
82. Davis R, Harsh K. Confronting barriers to universal screening for domestic violence. J Prof Nurs. 2001; 17 (6): 313–320.
83. Lanuza D, Davidson P, Dunbar S, Hughes S, De Geest S. Preparing nurses for leadership roles in cardiovascular disease prevention. J Cardiovasc Nurs. 2011; 26 (4 suppl): S56–S63.
84. McFarlane J, Symes L, Frazier L, et al. Connecting the dots of heart disease, poor mental health, and abuse to understand gender disparities and promote women’s health: a prospective cohort analysis. Health Care Woman Int. 2010; 31 (4): 313–326.
85. BC Centre for Disease Control. Harm reduction. Accessed June 12, 2012.

aAlthough often used interchangeably, for the purpose of this article, the terms abuse and violence will be termed abuse.
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abused women; cardiovascular disease; depression; gender; risk factors

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