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Neither Body nor Brain: Comparing Preventive Attitudes to Prostate Cancer and Alzheimer's Disease
Annette Leibing and Antje Kampf Body & Society 2013 19: 61 originally published online 19 March 2013 DOI: 10.1177/1357034X13477163 The online version of this article can be found at: http://bod.sagepub.com/content/19/4/61
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Article
Body & Society

19(4) 6191
Neither Body nor Brain: Comparing Preventive Attitudes to Prostate Cancer and Alzheimers Disease
Annette Leibing
University of Montreal, Canada
The Author(s) 2013

Reprints and permission: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1357034X13477163 bod.sagepub.com
Antje Kampf
University of Mainz, Germany
Abstract This article compares health promotion attitudes towards prostate cancer and Alzheimers disease. Our aim is to demonstrate that these two apparently distinct conditions of the aging body one affecting the male reproductive system, the other primarily the brain are addressed in similar fashion in recent public health activities because of a growing emphasis on a cardiovascular logic. We suggest that this is a form of reductionism, and argue that it leaves us with a dangerous paradox: while re-transcending, at least partially, the conceptual separation of body and brain, it clouds much-needed discussion and research, such as contingent issues of socio-economic and socio-cultural disease disparities. Keywords Alzheimers disease, body/brain, cardiovascular logic, prevention, prostate cancer
Two Organs and a Third A walk through a brain and a prostate is the title of a recent press release describing the larger-than-life interactive models of human
Corresponding author: Annette Leibing, University of Montreal, CP 6128, succ. Centre-ville, Montreal, QC H3C3J7, Canada. Email: annette.leibing@umontreal.ca http://www.sagepub.net/tcs/
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Body & Society 19(4)
organs used at the 2009 MEDICA exhibition in Du sseldorf, Germany (Heimann, 2009). The text describes the educational purpose of those models and mentions that only the heart could not be included in the event: given that a scale model of the heart would have to stand 4.5 meters tall, no room was high enough to hold it. The following year, however, the organizers explained that the heart would get its merited place of honor in the courtyard of the Du sseldorf congress center. While the title of the initial press release coincidentally mentions the two organs this article aims to discuss the brain and the prostate it is this third organ that occupies a place of honor in our analysis: the heart, standing for cardiovascular health, which we perceive to be increasingly central to current biomedical thinking. The romantic heart is often associated with an intuitive and true understanding of the world There is no instinct like that of the heart, said Byron and so can be broken with grief, perhaps through a lost love. A more contemporary correlation is made between stress and heart disease, a notion which has held since the 1950s (Rothstein, 2003).1 And while stress is a notion that mainly implies forces beyond ones control such as modernization, society, and work conditions cardiovascular health, as it is now often used in biomedical reasoning, is intrinsically linked to individual acts of prevention. As several authors have shown, lifestyle choices and behavior are ideally made by a responsible, reflexive individual the same individual that neoliberal regimes posit as the ideal citizen (Burchell, 1996; Castel, 1991; Crawford, 2006; Foucault, 1991; Greco, 2006; Petersen and Lupton, 1996; Rose, 1999a; Rose and Novas, 2005). Cardiovascular disease is generally described as an outcome of poor lifestyle choices, leading to conditions that involve narrowed or blocked blood vessels that can lead to a heart attack, chest pain (angina) or stroke. . . . Many forms of heart disease can be prevented or treated with healthy lifestyle choices.2 These conditions are central to what we call a cardiovascular logic. By this we mean a widespread and readily accepted etiological construct that explains a growing number of health conditions and not only heart attack, chest pain, or stroke most of which were previously considered separate pathologies. These conditions have become interconnected through a common underlying cardiovascular pathway that can hardly be distinguished from attitudes towards prevention. It is reminiscent of stress theory, set out in the mid 20th century, in its
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unspecific way of explaining almost everything (Viner, 1999). In this way, a cardiovascular logic draws attention to what we see as a specific biomedical reductionism3 which can be found circulating in a variety of texts and images, from the popular media to specialized biomedical publications. One example of this is the March 2010 issue of the German newsmagazine Focus (2010). In large font the headline on its title page states that not only behavior (here, diet) prevents the most diverse conditions, but that the underlying cause of all these conditions is of a cardiovascular nature: The heart diet: the right nutrition avoids cardiac disease, rheumatism, diabetes, and dementia. The growing importance of a cardiovascular logic does not replace genetics or the neurosciences two fields thought by many social scientists to dominate current biomedical reasoning, resulting in a pervasive genetic worldview (Petersen, 2006), neurocentrism (Pitts-Taylor, 2010), or brainhood (Vidal, 2009). Instead, we see the cardiovascular health paradigm as coexisting with, but increasingly dominating, health-related thinking, sometimes even effacing genetics and the neurosciences as explanatory reference points. As one Canadian nutritionist puts it: Im amazed by the number of people who blame genetics for developing disease. . . . Its as if it doesnt matter whether we . . . manage our weight, [and] eat whole foods . . . (Holly, 2005). An important value that comes with a cardiovascular logic is the idea of having control over ones health, in line with current notions of self-care in public health (Ziguras, 2004). In the field of genetics the more recent focus on epigenetics an antidote to the idea that we are hard-wired by our genes (Bird, 2007) has led, to a certain degree, to the idea that an individual can have control over relatively common causes of fatality due to genetic determinism. Geneticist Thomas Lerner, for instance, states that a number of studies suggest that epigenetic modifications impact behavior, and . . . those effects can be reversed (cited in Carey, 2010). In a similar vein, cardiologist Donald Lloyd-Jones writes that: health behaviors can trump a lot of your genetics. . . . This research shows people have control over their heart health (Northwestern University, 2010). Within the neurosciences, discoveries related to the plasticity of the brain (neuroplasticity), and the well-known mantra of brain training through regular activities such as completing crossword puzzles or learning languages (use it or lose it), now lead scientists to suggest that people can work on, and even have a certain control
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over, their own cognitive capacities. Yet, the certainty that people can prevent cognitive decline is being challenged by studies suggesting that these kinds of activities do not necessarily influence cognitive health (Pap et al., 2009). And, as will be shown below, neuroprevention is also increasingly linked to activities related to cardiovascular health. A cardiovascular logic further implies a new holism, because it transcends the more traditional division between mental and physical health reinforced in most biomedical realms. The ubiquitous example of exercise being generally associated with physical but not with mental health is now giving way as a result of this new holism to a belief that exercise impacts on conditions like depression or schizophrenia. Titles such as Walking away the blues: Exercise for depression in older adults (Dang, 2010; see also Mead et al., 2008) or Eat right, keep fit the number two prevention recommendation of the Canadian Mental Health Association (2010) show this change of mind.4 However, there is some evidence that a greater part of the putative therapeutic effect of exercise on depression is determined by patient expectations, ongoing symptom monitoring, attention, and other nonspecific factors (Blumenthal et al., 2007).5 In order to deepen our argument regarding the persuasiveness of a cardiovascular logic, we will provide a short discussion on some of the many origins of this logic, followed by a comparison of recent developments regarding two apparently very different conditions: Alzheimers disease and prostate cancer. Both conditions, when seen through the lens of a cardiovascular logic, lose their distinctiveness to a certain extent; they become different outcomes of a common etiological pathway. Beside the improvements that should come with being fit, slim and non-smoking, this pathway also reflects a number of interests unrelated to an improvement in health (such as a responsible individual becoming less dependent on state health provisions or showing an increased need for certain medications due to a strong emphasis on preventive pharmacological acts). The pathway further governs people in that new groupings of morally good and bad individuals come to life: these new emotional agendas (Rosenberg, 1997) differ from earlier moral ideas linked to health in that nowadays it is almost impossible to escape the responsibility to stay healthy. A cardiovascular logic, we argue, is creeping into every corner of reasoning regarding health problems. Its moral impact is becoming
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unavoidable: Unlike geneticism or neurocentrism, which still involve a measure of fate (ultimately we are not responsible for our genes or brains), a cardiovascular logic leaves us almost no more opportunity for just being sick (except maybe with a broken ankle). The following comparison is based on data stemming from the two authors long-standing research on Alzheimers disease and prostate cancer, in which both have analyzed the sources of change regarding each condition. Relying on this previous work, in which we applied some of the principles of discourse analysis to relevant documents, our aim is to construct parts of the recent history (see Rose, 1999a, 1999b) of the cardiovascular logic as an important paradigm in current public health. And although those kinds of data are not explicitly used in this article, insights exposed in earlier publications on Alzheimers disease certainly did draw upon empirical data stemming from fieldwork in different clinical and national settings. We are aware of the situatedness of biomedical facts, but our aim here is to show a general trend that influences, to different degrees, an increasing number of individuals around the world. Even when we identify specific, seemingly isolated examples (such as the German exhibition noted above), we see them as local manifestations of this general trend. The Multiple Origins of a Cardiovascular Logic A number of authors have described a new paradigm of health (Moore, 2010) or a new public health (Petersen and Lupton, 1996), starting more or less in the 1950s, a decade which saw a number of changes in attitudes towards health, such as the development of a risk factor concept and at-risk groups, along with an increased turn towards prevention with a specific focus on self-care and behavior (e.g. Rothstein, 2003; Timmermann, 2011).6 According to Armstrong (2009, 2010), the idea that behavior is a medical problem gained currency at this time, when it started to become linked to an individuals agency and was situated as a central target of health interventions (similar to lifestyle a notion that appeared at the end of the 1970s in western medical texts). During the 1950s, a growing concern with human behavior (e.g. Konrad Lorenz on aggression; Alfred Kinsey on sexual behavior) paved the way for landmark studies such as Friedman and Rosenmans (1959) research on the role of
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cholesterol in narrowing coronary arteries, which was then reformulated in terms of human behavior (e.g. type A behavior). The widely cited Framingham Heart Study (cf. Levy and Brink, 2005; Oppenheimer, 2005), initiated in 1948, when little was known about the causes of coronary heart disease, had an important impact on biomedical reasoning (see Mullner, 2007; Timmermann, 2006; Riska, 2000).7 In the 1980s particularly in North America a major concern was the adoption of a low-fat diet to prevent heart disease (a movement which actually began in the 1940s): Many Americans subscribed to the ideology of low fat, even though there was no clear evidence that it prevented heart disease. . . . Ironically, in the same decades . . . Americans in the aggregate were getting fatter, according to historian of medicine Ann La Berge (2008). This lifestyle correctness movement (Leichter, 1998), which in the last century was only promoted by those standing at the margins of biomedical thinking (such as naturopaths), has within the last few decades become cutting-edge biomedical science merging in part with an underlying contiguous sympathy for such approaches within the popular realm of medicine. Another reason why a cardiovascular logic has become so comprehensively accepted in recent years is economic: fears that national health systems would no longer be economically viable has inspired awareness campaigns emphasizing prevention through individual lifestyle changes the dropping of bad habits (Moore, 2010). This trend was eagerly picked up and nurtured by major pharmaceutical companies. As Jeremy Greene (2007) and others argue, pharmaceutical enterprises promoted and redefined a number of health conditions, especially previously untreated, often asymptomatic and flexibly defined conditions such as hypertension and diabetes (two conditions at the core of the American Heart Associations [2010] recommendations) because of their direct link to bad heart-health. In fact, a cardiovascular logic is also implicated in the marketing of new drugs and the reconceptualization of older ones, especially as prevention. One example is statins cholesterol-lowering medications which are theoretically ideal for a general prevention of ill-health, based on a cardiovascular logic. Statins are currently the most widely prescribed medication group in the United States. However, [c]holesterol medications . . . may not be as safe as preventive
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medicine as previously believed for people who are at a low risk of heart attacks or strokes (Wilson, 2010). The strong emphasis on selfgovernance through prevention within a cardiovascular logic, in combination with a general message of control over ones health, is tightly linked to pharmaceutical marketing regarding drugs that now need to be taken for an extended period: not only by individuals singled out as being at risk, but increasingly by whole populations that might be at risk (see Armstrong, 1995; Dumit, 2010). The recent suggestion to hand out statins in fast-food chains in order to prevent the cardiovascular risk of unhealthy eating is an example of this general attitude towards extended prevention (see Ferenczi et al., 2010). This turn towards primary prevention lies at the center of our comparative analysis of Alzheimers disease and prostate cancer. Alzheimers Disease and Cardiovascular Logic A recent book, Defying Dementia, written for the general public by neurologist Robert Levine (2010), exemplifies the emergent cardiovascular logic in relation to Alzheimers disease. Levines argument is that accelerated brain aging and neuronal damage become more accentuated through diabetes, obesity, hypertension, elevated cholesterol, smoking, excessive alcohol and drugs. In the afterword, Levine summarizes his arguments: Preventive measures should be thought of as a three-legged stool needing all three legs to hold any weight. The three legs are exercise, cognitive activities, and diet (2010: 21011). The excitement about prevention as a new focus in dementia care research can be found in a number of recent initiatives. One of them was the 2009 conference on Pathways to Prevention, organized by the International Psychogeriatric Association, which took place in Montreal. The organizers noted that there was a sense of being at the beginning of a new era in geriatric psychiatry in which prevention is becoming an increasing focus (Rapoport and Mulsant, 2010). Older publications on Alzheimers disease paint a different picture one that is brain-centered, and in which, as a result, prevention and cardiovascular risk factors have no place. Probably the first North American guide on Alzheimers disease for the general public, written by psychiatrist and geriatrician Barry Reisberg in 1981, does not even mention the words prevention and lifestyle. For Reisberg
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and his contemporaries, Alzheimers disease was a degeneration of the aging brain, and only interventions targeting brain biology and chemistry were conceivable treatment options. Cardiovascular factors played a role within the then carefully distinguished category vascular dementia a common division still in use, although the boundaries between the two diagnostic categories have become increasingly porous. Many specialists now practically merge these two conditions, or speak of dementia as one category, instead of setting up a clear division: vascular dementia versus Alzheimers (e.g. Kalaria, 2010).8 It is ironic that when awareness about Alzheimers started to grow (in the US this happened in the 1980s), older notions of atherosclerosis were deemed ignorant by those raising the profile of this disease of the century (Campbell, 2004; see also Reisberg, 1981: 15). Today, however, dementia is in large part becoming atherosclerosis again. Until the 1960s, dementia in elderly individuals was usually called arteriosclerotic dementia, a name introduced by Binswanger at the end of the 19th century to define a condition of cognitive decline secondary to the atherosclerosis of cerebral vessels (Battistin and Cagnin, 2010). In 1974, neurologist Vladimir Hachinski criticized this as misleading, and proposed the term multi-infarct dementia (MID), introducing the idea that cognitive decline needed an accumulation of cerebral infarcts. Alzheimers disease, however especially following the influential UK Newcastle study conducted by neurologist Martin Roth and his colleagues (e.g. Roth et al., 1966) became a separate entity seen as based on brain degeneration and its biological markers (especially plaques and tangles). Could HDL cholesterol the good kind linked to lower heart disease risk also protect people from dementia? was the question posed in a recent New York Times article (Rabin, 2010), a question answered by recourse to the same logic set out in the Levine book.9 This logic is even having an impact on non-medical fields, such as the new generation of motion games that follow the model of Nintendos Wii. The Microsoft Kinect program called Body and Brain Connection is, in the publishers words, a prevention program based on research that has shown that not just puzzles . . . can help your brain, but if you add a physical element [i.e. exercise] to that, it can jumpstart it and have even better, and more fun, results (quoted in Snider, 2010).
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In fact, the correlation between cardiovascular risk and dementia has been noticed before, but only now has it received particular attention from researchers. The APOE (apolipoprotein E) gene, and especially its allele E4, (e.g. Slooter et al., 1997; Tanzi and Parsson, 2000), understood to elevate the risk of developing dementia, is also involved in heart disease APOE is responsible for the transporting of fat in the body. This causal relationship had been already identified in the 1980s (e.g. Yamamura et al., 1984), but was widely ignored until 1993, when Duke University neurologist Allen Roses (2006) described the heterogeneity of APOE and its link with sporadic Alzheimers (the most common form, in which heredity plays less of a role than in the rarer, familial form). Nevertheless, although there were earlier recommendations regarding dementia and lifestyle (e.g. Friedland, 2001), only in the last few years has this become more commonplace. The question is: why is it only now that this existing knowledge has become salient (cf. Daston, 2000: 69)? One reason might be that in the 1990s, when Roses established the link between cardiovascular factors and dementia, hope for salvation through the new cholinesterase inhibitors was growing: in 1993, Tacrine, the first Alzheimers medication, arrived on the market. Tacrine, and to a certain degree also its four successor drugs, has recently lost a greater part of its credibility (see Leibing, 2006, 2009a, 2009b). However, now that prevention has become a well-accepted issue in dementia research, already existing drugs, or drugs with similar mechanisms, can be (re)marketed (see Cyranoski, 2011), while statins and other drugs influencing cardiovascular risk factors can be offered as additional treatment options (Sparks et al., 2010). The recently developed Dubois criteria, dividing Alzheimers disease into three phases (Dubois et al., 2007, 2010), are among the many mechanisms that helped to embed (Latour, 2000) a cardiovascular logic into scientific reasoning. For many years at least since the 1960s (e.g. Kral, 1962) the concept of mild cognitive impairment (MCI) was loosely attached to dementia, indicating a transitional period between normal ageing and the diagnosis of clinically probable very early Alzheimers Disease (Petersen, 2004). This concept, with its well-known limitations of predictive unspecificity (not all individuals with memory problems develop dementia later on; cf. George and Whitehouse, 2009),10 and the concomitant
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danger of a pathologization of normal forgetfulness, has now become officially accepted as a second phase of dementia. A third, preclinical phase even more preclinical than MCI is especially relevant for the discussion of a cardiovascular logic:
[L]arge cohort studies have implicated multiple health factors that may increase the risk for developing cognitive decline and dementia thought to be caused by AD. . . . In particular, vascular risk factors such as hypertension, hypercholesterolemia, and diabetes have been associated with an increased risk of dementia. (Sperling et al., 2011: 282, emphasis added)
This third stage, after Khachaturian (2011), has . . . brought the field to the threshold of a new frontier the struggle toward primary prevention. And in fact there has recently been an abundance of new ways of predicting and preventing dementia, not only through genetic testing. The American Alzheimers Association founded the Alzheimers Early Detection Alliance (AEDA), which is designed to educate people about the signs of Alzheimers, the importance of early detection and the resources available to help them (Alzheimers Association, 2010). A Globe and Mail article on the different ways to ensure early detection of Alzheimers risk declared:
It is also possible that early diagnosis may help patients make lifestyle changes that delay the onset of the disease. Studies suggest that exercise and a healthy diet may be protective. Both measures are widely advocated by doctors to prevent heart disease and stroke. (McIlroy, 2010)
The idea that a preclinical condition needs to be made concrete and detectable simply in order to exist can be shown by the extent to which the discussion about the Dubois criteria centers on biomarkers. The revision of the diagnostic (and research) criteria for Alzheimers disease is largely discussed in terms of visibility, such as brain scans (e.g. PET amyloid imaging) that reveal structural changes, and test results that show the presence of biomarkers visible under the microscope. For example, Janssen Pharmaceutica, together with GE Healthcare, announced in December 2010 that they were developing a non-invasive assay for detecting biosignatures (the beginnings of the formation of two biomarkers, amyloids and tau-tangles) to facilitate early diagnosis and intervention (Johnson & Johnson, 2010). The Australian Imaging Biomarkers and Lifestyle Study revealed the
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importance of visibility, and demonstrated the growing emphasis on lifestyle (see Sperling and Johnson, 2012). Early detection in the preclinical phase was also the target of the professorship for the prevention of dementia and Alzheimers-related diseases, financed by Pfizer Pharmaceuticals at Montreals McGill University (Pfizer, 2010). Pfizer announced that, together with the company DiaGenic (see DiaGenic, 2010), it was developing a technology that identifies blood-based biomarkers for early onset of Alzheimers disease. If successful, this would certainly mean earlier (and therefore longer) use of the already existing dementia drugs, such as Aricept (see AllBusiness, 2007). These changes in understanding dementia may also influence an important ethical discussion. For a long time, a heated debate existed about whether early signs of dementia risk particularly risk revealed by genetic testing should be revealed to the affected individual and her family. While some argued that results should be made known, so that necessary precautions could be undertaken (e.g. the last will and testament, or other legal and emotional acts), others argued that, since nothing curative could be done, and because the revelation could lead to discriminatory practices (e.g. by insurance companies), social stigma, depression, or even suicide, doing so would only cause distress. This is quite apart from the fact that even for the familial form of Alzheimers, genetics cannot predict with certainty whether dementia will happen (see Pedersen, 2010). With the emergence of a cardiovascular logic regarding dementia, however, concrete preventive measures could now be undertaken; therefore, revealing the identification of vulnerability early would mean that individuals could actively engage in diet and other lifestyle changes, as Gauthier et al. (2011) suggested:
In any case, the presence of [first] memory complaints offers an important opportunity to review cardiovascular risk factors, and counsel the individual on healthy lifestyle issues including tobacco cessation, regular physical and mentally stimulating activities which together may help deter the onset of dementia.
These recommendations are not completely disease-specific; they can be found targeting a number of health conditions. In the following section we will show an almost identical prevention rhetoric regarding prostate cancer.
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Prostate Cancer and Cardiovascular Logic Visiting the website of the American Cancer Society (2011), one will find under the guide to prostate cancer the heading prevention, in which one learns that [s]cientists have found some substances in tomatoes (lycopenes) and soybeans (isoflavones) that may help prevent prostate cancer. In a similar vein, medical information provided by the Mayo Clinic website advises visitors that they may reduce . . . [their] risk of prostate cancer by making healthy choices, such as exercising and eating a healthy diet (Mayo Clinic, 2011), although it cautions that theres no proven prostate cancer prevention strategy. There is now an abundance of popular manuals on prostate health, which specifically spread the word on nutritional guidance and lifestyle behavior changes, encouraging men to regain Prostate Power (Nixon and Gomez, 2007: 19; see also Mroz et al., 2011). The role of lifestyle in cancer prevention has been well documented (Bekkering et al., 2006; Chan et al., 2005; Czene et al., 2002). What is noteworthy at this point is that approaches to prostate cancer, which have so far been dominated by medical solutions and interventions with a focus on therapy, are now also emphasizing primary prevention (Kampf, 2010)11 based on a cardiovascular logic. This trend has not always been especially overt. The reinvention of multi-causal explanations of the emergence of cancer including, for example, nutritional and dietary approaches in the 1960s that were in line with the establishment of chronic disease epidemiology (Cantor, 2007: 23) triggered a public and academic debate about possible risks stemming from environmental and/or behavioral factors (such as nutrition). However, this relationship was not addressed in connection with prostate cancer, which remained out of the spotlight (Kampf, 2009), while more visible cancers (which also targeted younger patients), such as lung and breast cancer, received the immediate attention of the early anti-cancer campaigns (Aronowitz, 2009; Bell, 2010). Studies on prostate cancer and health disparities have only recently been published (e.g. Gilligan, 2005; National Cancer Institute, 2012). Throughout the 20th century, early detection and treatment were portrayed as forms of cancer prevention (effectively secondary prevention), and prostate cancer was no exception. The focus on preventing
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the dire consequences of late-stage prostate cancer involved finding ways to stop it from becoming fully developed: secondary prevention tests (e.g. rectal examinations, PSA tests, urine tests, and biopsies) have now become central to medical dealings with prostate cancer.12 However, diagnostic tests (such as microarray and PSA) have been repeatedly questioned by health professionals, especially because of over-diagnosis and consequent unnecessary treatments. In fact, by 2011, the United States Preventive Services Task Force recommended no screening for healthy men, including men of African-American background (identified as having an increased risk of disease incidence and mortality; Harris, 2011). The advent of screening tests does, however, illustrate the rise of neoliberal health policies, with a shift in responsibility for provision of health from the state to insurers (Rose, 1999a, 1999b) a responsibility which was then passed on to the medical profession. The preventive approach to prostate cancer has recently been driven forward and refined by two new concepts that draw on existing detection technologies: Watchful waiting (WW) for older patients (above 65 years of age) and active surveillance (AS) for younger patients. These concepts have not been without controversy, given that in the US few health care professionals recommend WW or AS as viable options, even though they are endorsed in other countries, such as Germany. Studies have suggested, however, that despite these academic controversies, men have been receptive to these preventive technologies for making sense of their uncertainty (Bell and Kazanjian, 2011; Kampf, 2010). This has led to men taking a stronger participatory role in their prostate health (Davison and Goldenberg, 2011). Today, primary prevention privileges a cardiovascular logic, as we have seen. This approach is currently entering prostate cancer discourses, a noteworthy development given the hitherto predominant focus on secondary prevention. The so-called metabolic syndrome, the apparent scourge of the 21st century, which includes obesity, Type 2 diabetes, high blood pressure, and dyslipidemia, is now linked by some researchers to failing prostate health and the development of prostate hyperplasia (understood to be a possible risk for the onset of prostate cancer). Studies recently conducted seem to suggest a link between the metabolic syndrome and high-grade Gleason scores (a histological staging characterizing cell differentiation,
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thereby indicating tumor presence) found in cell cultures taken from prostate biopsies (e.g. De Nunzio et al., 2011). Obesity is now seen as a risk factor for coronary heart disease, both in health care and health promotion debates in the United States and Canada (Fletcher, 2010; WHO/EU, 2006), but it is also linked to the risk of prostate cancer. This is because western high-fat diets and sedentary lifestyles affect hormone levels that are considered crucial in the disease progression of prostate cancer.13 In turn, an increasing number of studies promote the potential benefits of certain nutritional agents and compounds, such as green tea, isoflavone, lycopene, cruciferous vegetable, and omega-3 polyunsaturated fatty acid in the prevention of prostate cancer (Hori et al., 2011; Richman et al., 2011; for a critical discussion see Lippman et al., 2009). Bodily fitness, previously associated with primary prevention approaches in cardiovascular health campaigns (and in other cancer types), has now filtered into campaigns for the prevention of prostate cancer. Exercise may be good for the prostate as well as the heart. New research shows [that] older men who exercise regularly have a much lower risk of dying from prostate cancer, suggests one researcher (Warner, 2005). One important line of research currently entertains the idea of advocating male pelvic health: encouraging men to reduce the possible risks of urinary tract infections and erectile dysfunction and possibly prostate cancer by exercising (Kaplan, 2007). Standard procedures for treating men identified as having a genetic predisposition to the disease, which included active surveillance and early surgery or radiation (similar to the preemptive strikes used in breast cancer prevention; see Lo wy 2010), have gradually been rejected. A UCLA study has summed up the widening possibilities now open to (aging) men: prostate cancer can be prevented not only through risk education and by embracing testing for early detection, but also by eating a healthy diet, watching cholesterol levels and taking exercise (Giovannucci et al., 2005; see also Johnsen et al., 2009; Moore et al., 2009). The forcefulness of the new cardiovascular focus, as it affects prostate cancer and lifestyle, is illustrated by how quickly it has been taken up beyond its origins in North America. The US has generally been much more persistent in its debates about obesity and cholesterol levels than, for example, Europe, but we can now detect a profound shift from secondary to primary prevention in Europe as
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well. For example, the Austrian urologists association encourages its members to advise their patients on behavior, lifestyle, and nutritional changes as part of a primary preventive approach, a concept trademarked as Androcheck (Berufsverband o sterreichischer Urologen, 2007). This recent shift from secondary to primary prevention within health promotion and medical research is, however, still very much in the making and in part inconclusive: researchers have not established a direct link between obesity and the metabolic syndrome and incidence of prostate cancer (Dimitropoulou et al., 2011); likewise, there is not yet a proven causal connection between antioxidants and the lowering of prostate cancer risk.14 The parallels between Alzheimers and prostate cancer and a cardiovascular logic may seem unlikely. But they can also be illustrated by the emergence of new preclinical conditions: what certain social science studies have called a pre-disease state. These factors have lowered the threshold for intervention (cf. Aronowitz, 2009: 426; Lo wy, 2011). Researchers are looking for precursors to Alzheimers disease, and a condition called high-grade prostatic intraepithelial neoplasia (HGPIN) has been identified in relation to, and is characterized by, cellular proliferations similar to those seen in prostate cancer. Arguably, HGPIN serves as a mechanism that, just like the Dubois criteria for Alzheimers disease, helps to embed (Latour, 2000) a cardiovascular logic into scientific reasoning. Evidence supporting the relationship between HGPIN and prostate cancer has come from immunohistochemical, morphometric, molecular, and genetic studies. HGPINs presence is not established by PSA tests, but with biopsies. It does not come without controversy, however. There is a decided lack of knowledge on the timing of transformation into prostate cancer, and so HGPIN comes with never-ending surveillance circles (i.e. repeat biopsy 06 months after initial biopsy, then every six months for two years, and then every 12 months for life). The classic treatment strategies of prostatectomy or radiation are contra-indicated as of yet, but at-risk men (i.e. showing HGPIN) are advised to partake in clinical trials of chemopreventive agents (Cheng et al., 2004). A number of research studies are now investigating the efficacy of antioxidants, statins, catechins, and natural compounds (Bettuzzi et al., 2006; Ozten-Kandas and Bosland, 2011), as well as medications
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belonging to a drug class called 5-alpha-reductase inhibitors (5-ARIs), which are currently recommended for preventive treatment by the American Society of Clinical Oncology and the American Urological Association. The increase in health promotion, coupled with the promotion of primary prevention as a new means to deal with the threat of prostate cancer, is inseparable from a multimillion dollar industry addressing an anti-aging market, largely catering to aging (and prosperous) baby-boomers who care about their lifestyle choices (Kampf and Botelho, 2009). At times the advice given by the anti-aging advocates is paradoxical. Since the 1980s, the use of an estrogenicandrogenic hormonal substitute (Gynodian Depot [DHEA]) a product now available in supermarkets in the US has been recommended for strengthening the vitality and good health of members of the third age, but hormonal substitutes have started to come under scrutiny for possible connection to prostate cancer (Wagener, 2004). This scrutiny has in turn resulted in the development of new markets, such as plant technologies (intended as food additives to produce high levels of cancer-preventive agents), or as pharmaceuticals alongside already existing dietary supplements (nutriceuticals). This follows Isabelle Fletchers argument that there has been no simple shift from older, public health, environmental responsibility to new individual responsibility for preventing the onset of disease, but that what we are witnessing is predominantly the expression of environmental concerns about food consumed (Fletcher, 2010: 76). Advanced age remains the most well-established risk factor for prostate cancer (and Alzheimers): by age 70, about 65% of men have at least microscopic evidence of prostate cancer. Nonetheless, the current trend in preclinical diagnosis (and treatment) has shifted this focus to younger men (typically above age 30). This is despite the fact that prostate cancer usually grows very slowly, and older men with prostate cancer typically die of something else (see note 10). Yet, of course, the lowering of the diagnostic threshold has also lowered the mean age of diagnosis and intervention. Discussions about the adverse effects of PSA screening for older men now touch upon its possible benefits for younger men (Harris, 2011), who, as some argue, are also easier to encourage to make lifestyle changes.
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So What? Some Heartless Conclusions We have juxtaposed two diseases (or syndromes) in order to show an emergent and all-encompassing, commonly held reasoning we have called a cardiovascular logic. While this logic is applicable to a number of syndromes, Alzheimers disease and prostate cancer are ideal types in that they are both typically found in older individuals who are also at greater risk of cardiovascular diseases. In a world that is aging in an unprecedented way, arguments insisting on the urgency and importance of such reasoning are easily made and communicated. In both cases it could be shown that a cardiovascular logic widened the field of targeted individuals: Younger at-risk individuals are now being linked to what were once deemed diseases of aging through a newer emphasis on primary prevention. Studies on other age groups, for instance the childhood obesity epidemic and the discussion around the use of statins for children, would provide substance for further studies eventually providing data on how a cardiovascular rhetoric might transform future children into preventing individuals. The fact that Ritalin is now also being marketed as a treatment for severely obese children shows, once more, the widening of the scope of certain medications due to a cardiovascular logic. Without disputing the important task of developing ways to detect disease onset and progression early or, ideally, even to prevent disease we see the current turn towards primary preventive approaches (sometimes merging with secondary prevention) under the banner of a cardiovascular logic as problematic. The oversimplification of complex disease pathways close to what Narayan (2010) has called a risk factor silo not only hinders research on other biological mechanisms, it also clouds a number of factors that transcend the purely biological. Ethnic, gender, and class issues drift out of sight (see note 7), the more that public health campaigns insist on a cardiovascular logic. For example, in prostate cancer research, explanations for the racial/ethnic disparities in the incidence of prostate cancer, with disproportionate numbers of African-American men developing the disease, are inconclusive. Recent quantitative studies suggesting genetic predisposition (and not life conditions, for example) paradoxically go hand in hand with newer recommendations against screening of all men, regardless of ethnicity (e.g. Cheng et al., 2009).
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Likewise, some have recently pointed to the narrow scope of the discussion on public health, with the result that environmental issues such as pollution have been widely ignored. This is the case for cardiac diseases in general (e.g. Reeves, 2011), as well as more specific illnesses, including Alzheimers disease (Morgan et al., 2011) and prostate cancer (Pedersen, 2010; Ramis et al., 2011). Refocusing on environmental issues would place more responsibility in the hands of governments, industries, and the medical profession responsibilities that easily get hidden with an emphasis on self-care. But what is most striking is that public health campaigns now target almost everybody through a unified cardiovascular logic. In fact, there is certainly a social preoccupation, inscribed in research and campaigns, with cardiovascular health and its concomitant health conditions. Studies on epigenetics, for example, link genes to environment, as do the new neurosciences in their emphasis on the social brain. Once individualized notions of risk become social questions, such as the finding that our peer groups are deemed responsible for whether we are fat or not (Is obesity contagious?; see Lopez, 2008). The recent mushrooming of so-called neighborhood studies encapsulates the rather simplistic public health idea that governments only need to build more parks and public markets in order to ensure that individuals will do more exercise, and eat more vegetables instead of fast food. However, the social in this health issue continues to be treated as a matter of individual behavior and willpower. We are not talking about the kind of medical reductionism that George Engel (1977) once accused of lacking a biopsychosocial component. What we believe is happening is the acknowledgment of the social context, which immediately gets retranslated into one basic biological mechanism. Further studies, we hope, will build upon our more conceptual discussion to provide more culture-specific data, showing how a cardiovascular logic is being integrated or contested in specific contexts, such as national public health campaigns, but also how it is used and retranslated by different local players: politicians, doctors, patient groups, researchers, and pharma-managers producing clinical guidelines, research protocols, and other relevant documents, and how these finally impact on individuals embodying such narratives of risk.
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Acknowledgements We would like to thank the Deutscher Akademischer Auslandsdienst (DAAD), the Canadian Institutes of Health Research (CIHR) and the Social Sciences and Humanities Research Council (SSHRC) for financing our research. We are also extremely grateful for the reviewers stimulating input. Notes 1. Historians have noted that the origin of correlating stress with heart dysfunction dates back to military medical dealings within conscription practices and warfare in the early 20th century (see Woolley, 2002). 2. See Mayo Clinic at: http://www.mayoclinic.com/health/heartdisease/DS01120 (accessed April 2011); see also Health Canada (2010). 3. Reductionism here means that a single explanatory system has become common sense, excluding other possible explanations due to its epistemological force. This does not mean that all explanations relying on reductionism are wrong. 4. This holism is drawing unwittingly on a connection established between body and mind within medicine that received a new twist with Cartesian thinking. For an introduction to the vast literature on the subject, see Hagner (2008). See also Ecks (2009). 5. However, a Cochrane review shows that [e]xercise seems to improve depressive symptoms in people with a diagnosis of depression, but when only methodologically robust trials are included, the effect sizes are only moderate and not statistically significant (Mead et al., 2008). 6. One of the reviewers pointed out that the focus on lifestyle shares many continuities with older, clean living movements such as the late 19th-century US efforts to control alcohol consumption, tobacco use, and female reproductive health (see Bell et al., 2011; Engs, 1991; Petersen et al., 2010). 7. The aims of early cardiovascular prevention campaigns were in part gender-specific, in that risk concepts were based predominantly upon a research focus on male patients (see Riska, 2000). Within the last two decades there has been a considerable effort to draw attention to a gender-specific
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preventative campaign against cardiovascular diseases, but we believe that a cardiovascular logic merges genderspecific issues (see conclusion of this article). For example, the specifically female symptoms of heart attack, or female smoking as related to higher prevalence rates of heart disease, we see as unifying acts. 8. Kalaria (2010: S74), writing about dementia in general, states that:
There is ample evidence to indicate vascular risk factors are also linked to neurodegenerative processes preceding cognitive decline and dementia. . . . Several modifiable risks such as cardiovascular disease, hypertension, dyslipidemia, diabetes, and obesity enhance the rate of cognitive decline and increase the risk of Alzheimers disease in particular.
9. Regular physical activity, in general, is believed to improve brain function, both by increasing blood flow to the brain and by stimulating the production of hormones and nerve growth factors involved in new nerve cell growth. Exercise also raises levels of good HDL cholesterol (Rabin, 2010). 10. It is interesting to read that George and Whitehouse (2009: 17) compare MCI with prostate cancer: When does a patient get prostate cancer? The abnormal cells that can be labelled cancerous are found in most men who die in late age most of whom will have neither been diagnosed in life nor suffered any consequences from the cells. On the basis of fairly nonspecific blood tests, some men will have had surgery that impairs their quality of life without clear evidence that the cancer would have been life threatening. 11. There are three levels of preventive medical strategies in public health. They are generally defined as: primary prevention (inhibiting the onset of disease altogether), secondary prevention (early diagnosis and screening measures to detect onset of disease before it becomes symptomatic), and tertiary prevention (aiming at reducing disability and restoring function once a person has been affected by disease). 12. This corresponds, in part, to the late 20th-century surgical options offered as preventive therapy in cases of genetic predisposition to breast cancer (Lo wy, 2010). The taboo and stigma of
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prostate cancer and the gendered aspects of the health-seeking behavior of men may have contributed to the slow development of preventive campaigns (together with the diseases unclear etiology) (George and Fleming, 2004: 3). Others point out that little has been done so far in terms of providing public health promotion for older men, with screening programs predominantly centered on female bodies (Aronowitz, 2007; Lo wy, 2007). 13. This is most often discussed alongside studies on the differences between the Asian diet and the US diet and the respective mortality rates of prostate cancer (http://www.unisci.com/stories/ 20013/0911013.htm; accessed 10 March 2011). 14. See www.cancer.gov/cancertopics/pdq/prevention/prostate/heal thprofessional#Section_101, www.cancer.gov/cancertopics/eat inghints/page3#C17 (accessed February 2011). References AllBusiness (2007) Early detection push. Available at: http://www. allbusiness.com/insurance/health-insurance-government-healthmedicare/6622991-1.html (accessed April 2011). Alzheimers Association (2010) Know the 10 signs. Available at: http://www.alz.org/alzheimers_disease_know_the_10_signs.asp (accessed December 2010). American Cancer Society (2011) Prostate cancer: Whats new in prostate cancer research and treatment. Available at: http://www. cancer.org/Cancer/ProstateCancer/DetailedGuide/prostate-cancernew-research (accessed January 2012). American Heart Association (2010) Cardiovascular disease and diabetes. Available at: http://www.heart.org/HEARTORG/Con ditions/Diabetes/WhyDiabetesMatters/Cardiovascular-DiseaseDiabetes_UCM_313865_Article.jsp (accessed October 2010). Armstrong D (1995) The rise of surveillance medicine. Sociology of Health & Illness 17(3): 393404. Armstrong D (2009) Origins of the problem of health-related behaviours: A genealogical study. Social Studies of Science 39(6): 909926. Armstrong D (2010) Is the focus on health-related behaviours a new phenomenon? An answer to Vallgarda (2010). Social Studies of Science 40(4): 615617.
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Annette Leibing is a medical anthropologist (PhD University of Hamburg, Germany) who first taught at the Federal University of Rio de Janeiro and is now a full professor at University of Montreal. She does research on topics related to aging, psychiatry, stem cells, and others many of these topics located in Brazil. Her most recent books are entitled Thinking about Dementia Culture, Loss, and the Anthropology of Senility (Rutgers University Press, 2006; co-edited with Lawrence Cohen), The Shadow Side of Fieldwork Exploring the Blurred Borders between Ethnography and Life (Blackwell, 2007, co-edited with Athena McLean), and a volume on technologies of hope (PUL, 2010, in French; co-editor Virginie Tournay). Antje Kampf (PhD Auckland, MA Cincinnati) is junior professor for gender aspects of the history, theory and ethics of medicine at the Johannes Gutenberg-University Mainz. She is the author of Mapping Out the Venereal Wilderness: STD and Public Health in New Zealand, 19201980 (LIT-Verlag, 2007) and Aging Men, Masculinities and Modern Medicine (Routledge, 2013; co-edited with Barbara Marshall and Alan Petersen), and has published on the history of public health, aging, and gender. Current research includes a book project on the historical epistemology of male infertility in Germany, a project on Representation of gender and concepts of prevention of cardiovascular diseases in Germany, 19492000 funded by the German Research Foundation, and a larger historical study Translating cancer to the public: practices of knowledge and cultures of prevention since the mid twentieth century (funding proposal submitted).

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Leibing and Kampf

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Leibing and Kampf

Body & Society 19(4)

Leibing and Kampf

Downloaded from bod.sagepub.com at UNIVERSIDAD DE CHILE on December 2, 2013

Body & Society 19(4)

Leibing and Kampf

Body & Society 19(4)

Leibing and Kampf

Body & Society 19(4)

Leibing and Kampf

Body & Society 19(4)

Leibing and Kampf

Downloaded from bod.sagepub.com at UNIVERSIDAD DE CHILE on December 2, 2013

Body & Society 19(4)

Downloaded from bod.sagepub.com at UNIVERSIDAD DE CHILE on December 2, 2013

Leibing and Kampf

Body & Society 19(4)

Leibing and Kampf

Body & Society 19(4)

Leibing and Kampf

Downloaded from bod.sagepub.com at UNIVERSIDAD DE CHILE on December 2, 2013

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