Risk and Biomedicalization

“Marking Populations and Persons at Risk: Molecular Epidemiology and Environmental Health” – Sara Shostak

Three questions guide Shostak’s chapter: how did molecular biomarker research emerge? How is molecular biomarker research applied in environmental epidemiology? And, what are the consequences of molecular biomarker research for the biopolitics of environmental health and illness? (142).

For clarification purposes, I’d like to first provide a few definitions.

1. A biomarker is defined by Hanson and Osborn as the “measurable characteristics that indicate normal biologic processes, pathogenic processes, or pharmacologic responses to therapy.” These can include physiological measurements (heart rate, blood pressure, and performance status), clinical chemistry measurements (cholesterol and other blood tests), protein measurements (antigens or hormones), and clinical images (like x-rays or mammograms).

2. Hanson and Osborn also write that molecular biomarkers are a newly emergent way of reading genes/genomes/chromosomes/DNA which can “provide scientists with a ‘parts lists’ containing instructions for how a cell builds, operates, maintains, and reproduces itself while responding to various environmental conditions.” Because of these advents provided by discovering and studying molecular biomarkers, “researchers now can approach questions systematically and on a much grander scale study all the genes expressed in a particular environment or all the gene products in a specific cell, tissue, organ, or tumor.”

3. The British Medical Journal defines epidemiology as “the study of how often diseases occur in different groups of people and why.” It is the “information used to plan and evaluate strategies to prevent illness and as a guide to the management of patients in whom disease has already developed.”

4. Molecular Epidemiology, first used in a 1973 publication, originally entailed the ways that “molecular biological techniques” are used “to study particular disease vectors or ‘agents’ of disease” (246). Now, molecular epidemiology can be used as indicators of “future events in human biological systems at the molecular or biochecmical level” (246). For example, this study by Carrilho et al. shows how patients undergoing haemodialysis therapy are at a greater risk of susceptibility for contracting Hepatitis B based on reading fluid contaminants. This example falls into line with understanding how molecular biomarkers can provide epidemiologists with not only a “means of more precisely identifying individual and subpopulation risks,” but also with a means of elaborating “precisely those pathways” of risk turning into reality (248).

Of particular concern to epidemiologists are the ways that biomarkers can be used to “ascertain three types of risk: environmental risks (exposures), acquired risks (effects of exposures), and inherited genetic risks (intrinsic genetic susceptibilities)” (243). Though there are historical efforts to identify, assess, and affect environmental risks, there is only more recently a shift from the outward to the inward. In other words, a connection is established between the environment and the inner-workings of the human body. As a result of this shift, distinctions between the following become extremely complicated:

· treatment and prevention and “risk reduction”
· public health and private choice
· the individual and the state
· knowing and governing
· biology and power
· thought and practice
· the present and the future

Shostak describes how one of the most useful shifts in studying molecular biomarkers is the movemement from looking inside the biological subject’s body to, instead, understanding the “chain of events leading from exposures to outcomes” (247). That is to say, epidemiologists can “make new claims about the relationships between conditions external to and processes inside of the body” based on tracing exposures and distinguishing how one “handles that exposure” (250).

The ultimate goal of researchers who investigate molecular biomarkers to transform their findings into actions geared toward public health, including prevention vis-à-vis “warning systems” which can identify, observe, measure, trace, understand, reduce, and contain exposure itself and/or risks of exposure. The object of analysis is “measurable objects inside organs, tissues, and cells” (253). 3 Types of these are: markers related to enzymes, markers of genetic difference, and markers of preexisting conditions (253). An important shift, then, not only takes place in looking to exposures instead of (or alongside) the inside of the body, but also takes place in the language employed to discuss these happenings: “You have emphysema,” thus, becomes “You’ve got one hundred thousand deformed proteins” (254). This language becomes one piece of a much larger puzzle that transforms persons into “subjects of self-surveillance and biomedical interventions” designed to minimize risk and to promote prevention (256).

A Case Study: “Breast Cancer Risk as Disease” – Jennifer Ruth Fosket



Fosket’s essay on breast cancer risk and disease is a useful case study to explore questions of molecular markers, risk, health, and biomedicalization. Fosket’s chapter is concerned with the role that pharmaceuticals and chemoprevention play in biomedical practices.

Chemoprevention “is the practice of ingesting pharmaceuticals or nutraceuticals to prevent disease” (331). Chemoprevention in terms of breast cancer is a recent advent, and as Fosket points out, “with biomedicalization, it is no longer necessary to manifest symptoms to be considered either ill or even ‘at risk’” (331-332). A state of normalcy no longer exists: everyone is now, somehow, not normal and, thus, is a pre-packed candidate for self-surveillance and/or health research.

In this framework, breast cancer becomes a fertile site for exploring question and controversies about how this all comes to be: to some extent, we are less concerned with treating and/or curing breast cancer. Instead, we are concerned with treating breast cancer risk. Risk not only undermines a state of normalcy and/or a state of being ill: risk itself becomes, simultaneously and paradoxically, the normalcy and the state of being ill and the disease itself. A few points become important:

First, chemoprevention for breast cancer (and, possibly other diseases) “enters the scene at a time when little else exists to prevent the disease (and, I would add, cure the disease) and uncertainty dominates the identification of breast cancer’s risks” (333). This is an attractive proposition because chemoprevention becomes a means to disguise or even replace efforts to cure diseases which might either be incurable or there is no real market interest in curing. All of this unfolds, as Fosket puts it aptly, “against a backdrop of uncertainty” (334).

Second, there is ambiguity about the word “prevention” and all that it can possibly entail. Primary prevention essentially refers to preventing the cancer in the first place, while secondary prevention involves detecting (i.e. “early detection) cancer at its earliest and most treatable stages (334-335). Betty Ford’s public breast cancer scare and mastectomy not long after her husband became president in 1974 is a key historical moment which points to the adoption of public language of “early detection.” In 1975, she gave a speech to the American Cancer Society, speaking candidly about her experiences: “I just cannot stress enough how necessary it is for women to take an active interest in their own health and body,” she said.

Third, the conception and implementation of tamoxifen, the only breast cancer chemoprevention drug approved by the FDA, is a viable example of the complicated distinctions between treatment and prevention. As an estrogen-mimicking drug, there have been a number of controversies related to tamoxifen. These include: how in the process of addressing one risk, another risk can arise; ethical questions about how you test drugs on healthy subjects; questions about how you select test subjects; the notion of “informed consent” and test subjects; the nature of warning labels; exclusion of certain groups of people in test trials; and so on.

In the end, tamoxifen was approved by the FDA, but not as a form of prevention: it was approved as a “risk reduction” (348). With the approval of tamoxifen, “treating risk with pharmaceuticals increasingly came to be seen as a legitimate, feasible, and worthwhile means of preventing disease both in the realm of breast cancer and more widely” (349).

Discussion Questions:

1. How do we communicate about risk? There are entire centers and areas of study dedicated to “risk communication.” What do you perceive to be the greatest challenges to communicating about risk and why?

2. Take a look at this website for a company called Pharmaceutical Product Development, Inc. Look over the information for clinical volunteers: who is eligible, what to expect, the testimonials of volunteers, etc. How does the language constitute the volunteer into a subject of the study and something beyond the study? What kinds of ethical questions are raised?