This week I developed hypertension, not because my blood pressure increased but because new guidelines lowered the threshold for defining what is abnormal. In the US, this has doubled the number of hypertensive women under the age of 45, tripled the number of hypertensive men under 45, and increased the overall rate of high blood pressure from a third to nearly half—and more than half for African Americans.
But will expanding the definition of hypertension, while keeping its prevention restricted to medications and individual “lifestyle changes,” help mass prevention?
Cardiovascular disease is the leading causes of death but is also preventable because it tends to develop after people have been exposed to risk factors for years. One of the main biological risk factors, high blood pressure, has been called the “silent killer” because people don’t experience any symptoms for years until they suffer a heart attack or stroke. The concern that our bodies are ticking time bombs frequently leads people to go the emergency department in the absence of any symptoms, just because their blood pressure reading is high. But as the saying goes, “treat the patient, not the number.” In the vast majority of cases, hypertension—in the absence of symptoms or signs of organ damage—is not an acute medical problem requiring immediate treatment, but a chronic risk factor requiring prevention.
For decades we’ve known that the risk of cardiovascular disease increases as blood pressure rises, and that normalizing blood pressure can lower the risk. But trying to prevent cardiovascular disease in a population by treating “high risk” individuals, without addressing what determines the population risk as a whole, runs into the problem inherent in this approach. As epidemiologist Geoffrey Rose explained in his article Strategy of prevention: lessons from cardiovascular disease,
“The preventive strategy that concentrates on high-risk individuals may be appropriate for those individuals…but its ability to reduce the burden of disease in the whole community tends to be disappointingly small. Potentially far more effective, and ultimately the only acceptable answer, is the mass strategy, whose aim is to shift the whole population’s distribution of the risk variable.”
But rather than expanding the approach to cardiovascular disease prevention in order to shift the whole population distribution of risk, guidelines have focused instead on expanding the definition of high blood pressure—labeling more people as “high risk” and in need of treatment.
Whereas hypertension was previously defined as 140/90 (“normal” being 120/80), the 2003 guidelines created the concept of “pre-hypertension”: blood pressure at the upper end of normal (120-139/80-89), which was at risk of becoming high blood pressure. In other words, “pre-hypertension” was a risk factor for a risk factor for a disease. While broadening the concept of risk, treatment remained the same: individual “lifestyle choices” like diet and exercise.
At the same time studies have found that intensive blood pressure lowering can reduce mortality rates in high-risk groups. Much of the discussion of the new guidelines quotes the 2015 SPRINT trial that reduced mortality by lowering blood pressure to 120. But this was in a selected group of patients with previous heart or kidney disease or other high risks, and the small absolute mortality reduction came at the cost of more emergency department visits for low blood pressure and kidney injury. Now this cost-benefit decision in a high-risk group of patients has been generalized to everyone—which will be eagerly received by pharmaceutical and insurance companies. In the same year as the SPRINT trial, the Journal of Insurance Medicine found that “switching to a ‘normal’ reference range of SBP<130 offers superior risk assessment relative to using BP<140/90.” In the latest blood pressure guidelines, “high blood pressure” has been lowered from 140/90 to 130/80, “pre-hypertension” has disappeared, and 30 million Americans have been labeled with a pre-existing condition. If this results in high premiums or reduction in health care coverage, the expansion of diagnosis in the interest of promoting health could could reduce access to healthcare or force more people to chose between medicine and food.
My blood pressure has consistently been in the 130s over 80s—and yet I’ve gone from having normal blood pressure, to having “pre-hypertension” and now having high blood pressure. But isn’t this extra vigilance needed if cardiovascular disease (CVD) continues to be the leading cause of death? As the guidelines state, “hypertension accounted for more CVD deaths than any other modifiable CVD risk factor and was second only to cigarette smoking as a preventable cause of death for any reason.” But the only risk factors considered modifiable are individual diet, exercise, and smoking/alcohol.
The definition of blood pressure has expanded, but the approach to prevention has not. As the former past president of the American College of Cardiology explained “an important cornerstone of these new guidelines is a strong emphasis on lifestyle changes as the first line therapy. There is an opportunity to reduce risk without necessarily imposing medications.” But as the guideline co-author explained, "Yes, we will label more people hypertensive and give more medication, but we will save lives and money by preventing more strokes, cardiovascular events, and kidney failure."
In other words, the only option we have to prevent cardiovascular disease on a population level is to label more people as at risk, and focus control on individual consumption and medicating our internal environment. There must not be any other modifiable risk factor, and nothing else we can do to stop the ticking time bomb. The “comprehensive” 500-page guideline has one paragraph on “environmental risk factor,” which it redefines as diet, physical activity and alcohol consumption. Factors in our external environment—including those that restrict consumption choices and access to medicine—must be irrelevant.
Embodying our world
But hypertension, cardiovascular disease, and every other health issue are not disembodied phenomena, arising spontaneously irrespective of context. As social epidemiologist Nancy Krieger explains, “we, like any living organism, literally incorporate, biologically, the world in which we live, including our societal and ecological circumstances…The concrete reality of embodiment in turn is expressed in biological characteristics, which exhibit both individual and population distributions.” Hypertension and its complications are not a purely biological phenomena but are intertwined with a number of social, economic and ecological silent killers.
According to last year’s World Health Organization report, Preventing disease through healthy environments: a global assessment of the burden of disease from environmental risks, a quarter of all global deaths are due to environmental factors. Modifiable factors such as air pollution, road traffic, occupational exposures, and high demand and low control work contribute to 35% of the total burden of ischemic heart disease and 42% of the total burden of stroke. Looking only at pollution as a cause of illness, this year’s Lancet commission on pollution and health found that “in 2015, all forms of pollution combined were responsible for 21% of all deaths from cardiovascular disease, 26% of deaths due to ischaemic heart disease, 23% of deaths due to stroke”. As it details, pollution influences every aspect of cardiovascular disease—from risk factors like high blood pressure, serum cholesterol and insulin resistance, to the development of atherosclerosis, to emergency department visits and mortality. Surely this should be included in a comprehensive assessment of how to prevent cardiovascular disease.
The disproportionate distribution of environmental pollution, precarious work and stress also help explain the disproportionate rates of high blood pressure in the Black community. Differential rates have been noticed for years but are often reduced to claims of racial difference. The Management of High Blood Pressure in Blacks guideline explains high rates of blood pressure by blaming cognitive factors like “nonbiomedical beliefs,” behavioural factors like less physical activity and bad diets, and physiological factors like different kidney function and salt retention. This focus on inherent biological difference has a long history. As White Coats for Black Lives explains, “biomedical research has historically characterized the very bodies of Black people as being the center of countless diseases, without thinking critically about how socioeconomic disparities and historical institutional discrimination have lead to the disproportionate amounts of disease observed in minority populations.”
Differential rates of blood pressure and other risk factors are not an indicator of inherent biological difference, but are embodied expressions of the totality of social, economic, and ecologic inequalities—which also constrain “lifestyle choices” and access to medicine. The result is higher rates of cardiovascular disease: the embodied experience of racism is literally heart breaking. As Krieger explained:
“Considering the public health problem of increased risk of hypertension in African Americans compared with white Americans, ‘embodiment’ reminds us that a person is not one day African American, another day born low birth weight, another day raised in a home bearing remnants of lead paint, another day subjected to racial discrimination at work (and in a job that does not provide health insurance), and still another day living in a racially segregated neighborhood without a supermarket but with many fast food restaurants. The body does not neatly partition these experiences—all of which may serve to increase risk of uncontrolled hypertension, and some of which may likewise lead to comorbidity, for example diabetes, thereby further worsening health status.”
In a study 20 years ago, she found that anti-Black racism and internalized oppression is a significant risk factor for hypertension: “the blood pressure differences we observed associated with reported experiences of racial discrimination, in conjunction with response to unfair treatment, are on par with or exceed those associated with other cardiovascular risk factors targeted for nonpharmacologic interventions (eg lack of exercise, smoking, and unhealthy high-fat, high-salt diets).”
This does not mean dismissing the power of medicine and the potential of individual choice, but empowering access to healthcare and individual agency by challenging their constraints. If we expand the definition of high blood pressure we should also expand the understanding of its broader causes, and if we lower the threshold for medical intervention we should also lower the threshold for social, economic and ecological improvement. As Rose explained in his book Strategy of Preventive Medicine,
“A population-wide approach can itself operate at either a more superficial or a more basic level. Health education is often only a superficial approach, when it seeks simply to encourage or persuade people to behave differently. A radical approach aims to remove the underlying impediments to healthier behavior, or to control the adverse pressures. The first or medical approach is important, but only the social and political approach confronts the root causes.”
Thankfully there are movements confronting anti-Black racism, climate injustice and precarious work—which can combine with healthcare to both treat the biological expression of high blood pressure and address the social, economic and ecological causes it embodies.