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Page 1Volume 20, No. 3 Public Policy & Aging Report

Volume 20, Number 3Summer 2010

Public Policy & Aging Report

A publication of the National Academy on an Aging Societya policy institute of The Gerontological Society of America

—Continued on Page 3

The Food Environment: Changing 50 Years of Growing an Inflammatory Diet..........................................................page 9

The Chemical Environment: Toxic Chemicals, Hazardous Substances, and Chronic Diseases of Aging....................page 16

The Psychosocial Environment: An Intergenerational Approach....................................page 27

Environmental Threats to Healthy Aging: An Ecological Perspective

Ted SchettlerMaria Valenti

Over the next few decades, the United States will see a dramatic increase in its aged population; the number of people age 65 and over will double by 2030. This profound demographic shift will influence almost all aspects of American life, including health status, health care, economics, and social structures. Although increased longevity in many ways represents success and offers exciting opportunities, it also poses tremendous challenges. Among them are the chronic diseases associated with aging.

The articles in this issue explore the effects of physical, nutritional, and psychosocial environments on the risk of acquiring many of today’s common diseases, even in people who are genetically predisposed. Although these environments largely are discussed separately, it is also important to integrate them into a more comprehensive eco-social or ecological model. Such a model can help us understand how environmental factors collectively influence health outcomes.

Moreover, many determinants of chronic disease patterns also are linked directly or indirectly to activities that drive climate change and general ecosystem degradation, such as traffic- and energy-related air pollution, air and water pollution associated with industrialized agriculture, and ecosystem

contamination with industrial chemicals, among others. Thus, interventions that address the structural, systemic origins of common chronic diseases also can benefit ecosystem health more generally, thereby linking healthy aging to planetary healing.

Here we describe select health trends of concern and an integrated model that accommodates multiple inputs and health outcomes in a causal web. We also highlight several integrating, biologic mechanisms common to the origins of many of today’s common disorders and conclude with general thoughts about response strategies.

We concentrate on obesity, diabetes, cardiovascular disease, metabolic syndrome, cognitive

The Built Environment; Planning Healthy Communities for all Ages: Community Design, Neighborhood Change, and Impact on Older Adults.................page 22

We Are What We Eat, Breathe, and Do

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decline/dementia, and Parkinson’s disease because they share underlying biologic pathways that can be altered inappropriately by environmental triggers. These were also the subject of an extensive recent review (Stein, Schettler, Rohrer, & Valenti, 2008). The analysis and model likely can be extended to various kinds of cancer, asthma, arthritis, and other degenerative diseases.

Disease Trends Obesity is a major public health threat in the

U.S. and in many other countries throughout the world as they adopt a Western lifestyle. Two-thirds of American adults are overweight and one-third is obese. Trends in most age groups are progressively upward. In the past 28 years, the prevalence of obesity in children ages 6 to 11 years increased from 6.5 percent to 19.6 percent, although this may recently have leveled off (U.S. Centers for Disease Control and Prevention, 2010). Childhood obesity disproportionately impacts low income and minority children. Obese youth are more likely than their non-obese counterparts to have risk factors for cardiovascular disease, such as high cholesterol or high blood pressure. Childhood obesity increases the risk of becoming an obese adult and therefore of experiencing obesity-related health problems later in life. According to a recent assessment, 32 percent of people age 65 and over are obese today, compared with 22 percent between 1988 and 1994 (The Federal Interagency Forum on Aging-Related Statistics, 2010).

Obesity is a risk factor for diabetes, cardiovascular disease, Alzheimer’s disease, some kinds of cancer, gall bladder disease, and degenerative joint disease. The origins of obesity are multi-factorial and include excessive caloric consumption and insufficient exercise, as well as a food production system that makes readily available calorie-dense, nutrient-poor foods. Relatively recent evidence suggests that industrial chemicals used in a variety of consumer products to which people are exposed regularly also may play a role (Stemp-Morlock, 2007).

Diabetes has become more prevalent in all age groups in the U.S. in the past 25 years. In 1980, fewer than three percent of the general U.S. population had diabetes compared to 7.8 percent in 2007 (U.S. Centers for Disease Control and Prevention, 2007).

Type 2 diabetes (non-insulin dependent) historically has been extremely rare among children, but in recent years it has become more common. Diabetes, too, has multi-factorial origins and shares many risk factors with obesity.

Cardiovascular disease incidence sharply increased during the middle of the 20th century, although related mortality has declined during the past 25 years because of a variety of medical and lifestyle interventions. Nonetheless, heart disease remains the leading cause of death in men and women in the U.S. Cardiovascular disease is linked to diet, smoking, cholesterol levels, hypertension, psychosocial stressors, air pollution, arsenic in drinking-water, mercury, and other environmental contaminants (Schettler, 2005).

Metabolic syndrome is a term that describes the clustering of various combinations of glucose intolerance, elevated insulin levels, abnormal blood lipids, hypertension, and abdominal obesity. Obesity, a sedentary lifestyle, inherited genes, the intrauterine environment, and environmental chemicals are likely to be involved in the origins of metabolic syndrome. Its presence increases the risk of developing type 2 diabetes and coronary artery disease. A number of studies conclude that metabolic syndrome in mid-life is a risk factor for cognitive decline and dementia. In the U.S., metabolic syndrome is present in nearly half of adults over age 60 and one-fourth of the population at large (Stein et al., 2008).

It is estimated that up to 5.1 million people in the U.S. have Alzheimer’s disease (National Institute on Aging, 2010), and current trends suggest this will nearly triple by mid-century. The impact on the health care system, families, and caregivers is enormous and will grow rapidly if the trend is not reversed. Similarities, differences, and overlaps between Alzheimer’s disease and dementia due to underlying vascular disease are somewhat unclear and are the subject of extensive research efforts. Older age is just one of many risk factors for Alzheimer’s disease and dementia more generally. Diabetes associated with a sharply increased risk of experiencing cognitive decline and dementia later in life, as are midlife obesity, elevated cholesterol levels, and metabolic syndrome. In addition to dietary influences on obesity and diabetes, many studies find that increased dietary saturated fat consumption increases the risk of dementia as much as two- to three-fold (Morris, 2009).

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Page 4 Volume 20, No. 3 Public Policy & Aging Report


exposures to lead, air pollution, other environmental contaminants, social isolation, and low socioeconomic status also increase risks. Thus, dementia is yet another condition in which environmental factors play an important causal role.

Trends in Parkinson’s disease are unclear because of the lack of good registries, but the risk of this disorder is also increased by certain environmental exposures. Genetic susceptibility seems to be a strong influence mostly in early onset Parkinson’s disease (before age 50), and even then, in all likelihood is in combination with environmental factors. But in more common, later onset Parkinson’s disease, environmental influences on the risk of developing the disorder are more prominent, perhaps through interaction with underlying susceptibility genes. Risk factors include exposures to certain pesticides, solvents, air pollution, and metals such as lead, iron, and manganese, among others (Stein et al., 2008).

An Ecological Health Framework

Health status depends on complex interactions among many entangled variables that are identifiable at many levels, including the individual, organ, cellular, and sub-cellular as well as the family, community, society, and ecosystem (see Figure 1). When we look, we often find influences of each of these among the others.

For example, lower socioeconomic status and some neighborhood characteristics are associated with higher levels of biomarkers of inflammation and an increased risk of coronary heart disease, independent of other risk factors such as smoking or diet.

Low-birth weight children have elevated levels

of markers of oxidative stress in their blood, and these changes appear to persist into later childhood. Low-birth weight children are also at increased risk of developing diabetes and obesity later in life, particularly if they experience early rapid catch-up growth. This generally is thought to be due to fetal programming that permanently sets neuroendocrine and metabolic systems in such a way that the fetus developing in a nutrient-poor environment is less able to adapt to abundant nutrition after birth. Some scientists believe that the changes associated with low birth weight also may increase the risk of Alzheimer’s

disease later in life. If this is true, then risk factors for low birth weight—for example, poor maternal nutrition, adverse maternal fatty acid profiles, young maternal age, cigarette smoking, air pollution, and living in poor neighborhoods, among others—may contribute to the risk of dementia in offspring decades later (March of Dimes, 2008; Ross, Desai, Khorram, McKnight, Lane, & Torday, 2007).

Thus, an ecological

framework has both space and time dimensions. It accommodates an expanded, interconnected worldview that includes multiple levels of analysis. It also acknowledges that an individual’s early and continued experiences can have strong influences on health status even decades later.

The fetal basis of adult disease is an area of intense research interest. This work was stimulated by the observation that suboptimal nutrition during fetal development and early childhood is associated with an increased risk of heart disease and stroke decades later (Barker, Winter, Osmond, Margetts, & Simmonds, 1989). More recently scientists have shown that

Figure 1 Ecological Model of Health and Disease

This model emphasizes the progressive nesting of individuals within families, within communities and finally within ecosystems. Variables at any level can influence directly or indirectly measures of health at any other level. Influences may be identifiable in individual markers such as blood pressure, arteriosclerosis, and inflammatory mediators, or they may be identifiable in neighborhood- or community-level markers such as disease patterns or socioeconomic gradient. The ecological framework implies far less distinct boundaries across levels than our medical, public health, and environmental health institutions generally acknowledge.

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this phenomenon extends beyond poor nutrition. For example, in laboratory rodents and primates, temporary low-level, early-life lead exposures cause increased activity of the gene that produces amyloid protein late in life (Wu et al., 2008). The pathologic plaques in the brains of people with Alzheimer’s disease consist of fragments of amyloid protein. This adds to the concern that the foundation for the disease in some people may be at least partially established decades before illness becomes apparent, perhaps even during fetal development or early childhood.

The ecological framework not only suggests new ideas for research but also for policy interventions likely to improve health. Since many features of the environment—beginning with fetal development and continuing throughout the lifespan—influence health status and disease risk later in life, efforts to prevent chronic diseases that tend to appear later in life must begin with conception and even in youth before they reach their reproductive years.

Integrating Biologic Mechanisms

Considerable evidence shows that inflammation and oxidative stress are involved intimately in the cascade of events leading to the onset of Alzheimer’s and Parkinson’s diseases (Stein et al., 2008). These biologic mechanisms are also relevant in cardiovascular disease, diabetes, and many kinds of cancer. Obesity itself is often characterized by chronic, low-grade inflammation, which helps to explain how being overweight increases the risk of various diseases in which inflammation plays a role. Insulin resistance, characteristic of type 2 diabetes, is also intimately associated with inflammation and oxidative stress. In sum, these are among common biologic pathways that

link different environmental variables with diverse health outcomes.

An ecological perspective reminds us that family-, community-, societal-, and ecosystem-level variables can pathologically up-regulate these biologic mechanisms, thereby influencing risk in individuals and patterns of disease in populations (see Figure 2). We also can see why patterns of disease may vary from one community or society to another. These patterns are established by the distribution of multi-level risk factors throughout a population, but an individual’s risk of a disease is influenced by individual susceptibility plus the specific aggregation

of risk factors in that person.

Multiple Influences Offer Multiple Intervention Opportunities

An ecological model and the complexity that it attempts to represent makes clear how challenging it can be to establish with certainty the origins of disease in an individual or in a population. This is particularly

true for multi-factorial diseases in which many different, multi-level environmental variables, interacting with susceptibility genes and with each other, influence disease risks and patterns (see Figure 3). The huge increase in lung cancer risk associated with smoking, which is hard to miss, is an exception. More commonly, diseases originate from conditions created by a more complex collection of interacting multi-level risk factors, each of which may have more modest influences than smoking does on cancer risk. This means that preventing or delaying the progression of these diseases will require steps to adjust the entire

Figure 2 Pathways to Health or Disease

Pathways to chronic disease can be replaced by pathways to healthy aging and resilience.

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array of intertwined risk factors in more favorable directions, without a high degree of certainty about the quantitative contribution of each one. And, it must be understood that some steps will need to be taken at the community and societal levels rather than focusing exclusively on individual lifestyle change.

When large numbers of the general population are exposed to an environmental hazard or conditions that confer risk, even small changes can translate into a large number of cases avoided. For example, modest improvements in air quality in many areas of the US would reduce total mortality and cardiovascular hospital admissions by tens of thousands each, since everyone in a community is exposed to the air and air pollution increases the risk of cardiovascular events and deaths with no evidence of a safe threshold (Brook et al, 2004).

Similarly, considerable evidence shows that exposure to certain pesticides increases the risk of Parkinson’s disease. Since a large portion of the general population is exposed to pesticides, particularly in agricultural communities where exposures to restricted chemicals are common within the general population, even if the increased risk on an individual level is modest, reducing exposures across the population likely would result in a significant decrease in Parkinson’s disease.

And, based on studies described elsewhere in this issue, it seems highly likely that population-wide shifts toward the Mediterranean diet would decrease

significantly the incidence of diabetes, obesity, cardiovascular disease, and Alzheimer’s disease. That does not mean that everyone eating a Mediterranean diet will be spared from these conditions. In some people, other risk factors may be determinative. But from a public health perspective, that kind of dietary modification is highly likely to be beneficial widely and can be supported easily by the evidence.

But we also know that simply making information available to individuals is not enough to foster dietary changes. The food environment, at community and societal levels, also must be addressed in order to decrease the availability and appeal of unhealthy food and make more nutritious food readily available and affordable.

Finally, the ecological framework reminds us that, in some people, single risk factors of modest importance can be much more significant when

they co-occur with others. For example, poverty, dietary iron deficiency, and lead exposure are independent risk factors for cognitive impairment in children. But, when they occur together, each increases the impacts of another. Similarly, higher levels of life-long exposure to lead increase the risk of dementia. That effect is magnified in elderly people living in neighborhoods with little social cohesion that generate stress and safety fears.

The good news is that numerous contributing factors provide multiple entry points for beneficial interventions at every level. For

Figure 3 Multi-Level Interacting Contributors to Neurodegeneration and Other Chronic Diseases

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example, increased exercise and decreased caloric intake will help to reduce obesity, which in turn reduces diabetes and dementia risks. Individual behavioral change is one way to approach this, but communities also can make certain that sidewalks, bicycle paths, parks, safe neighborhoods, and nutritious foods are available and their use is encouraged. And, when we begin to think routinely of sustainably produced, nutritious food in neighborhood markets, farmers markets, schools, and hospitals as a way to reduce the burden of diabetes, heart disease, obesity, dementia, climate change, and air and water pollution, we will have connected a few of the dots.

In complex systems, although we can never predict with certainty the extent to which interventions will be beneficial or even will have unintended adverse consequences, we can be guided by principles, available evidence, and ongoing monitoring. No single strategy is likely to be enough. Multi-level interventions will be necessary and will vary from place to place. It may take time to see results, but this should not be used as an excuse to delay.

The biomedical model of disease and treatment emphasizes pharmaceutical and lifestyle interventions in individuals and, to some extent, in families. A public health model puts more emphasis on community-level disease prevention and early diagnosis. An ecological model looks even more broadly at system conditions that foster health or disease and explicitly recognizes the intimate connections among human communities and the natural world.

Primary Disease PreventionStrong arguments support raising

primary disease prevention to a much higher priority than is reflected in current policies that overwhelmingly direct resources toward early diagnosis and treatment. Primary prevention can have a large return on investment and reduce the environmental and public health impacts of the healthcare industry itself. The health care sector, now accounting for 17 percent of the gross domestic product and steadily growing, is second only to the entire food industry in intensity of energy consumption and is a significant emitter of greenhouse gases.

Many of the drivers of today’s chronic

diseases are also responsible for widespread degradation of ecological systems on which life depends. For example, our food production, processing, transportation, and distribution systems supply an abundance of relatively cheap calorie-rich, nutrient-poor food, fueling an epidemic of obesity, diabetes, heart disease, and dementia, while contributing to widespread air and water pollution, including large marine dead zones. Long-term human existence will require living within the regenerative capacity of the biosphere. Objective data overwhelmingly support the conclusion that human activity on the planet already exceeds that capacity and has for some time (Millennium Ecosystem Assessment, 2005).

We are entering an unprecedented period of global triage necessitated by the way that humans live on the earth. No sector of society or institution can ignore these issues as they plan future activities. As our population ages and faces the chronic diseases of our time, we also can think about our obligations to future generations and the quality of the world we will leave to them. We must seize opportunities that will improve our own health and the health of the world’s ecosystems, thereby increasing the chances that our grandchildren and great-grandchildren also can flourish.

Ted Schettler, MD, MPH, is science director of the Science and Environmental Health Network and a co-author of Environmental Threats to Healthy Aging. Maria Valenti is program director of Greater Boston Physicians for Social Responsibility and a co-author of Environmental Threats to Healthy Aging.

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