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Cardiovascular disease (CVD) is a persistent and chronic health problem in the United States. As the leading cause of death for nearly 50 years, in 2005 CVD was responsible for over 850,000 deaths in adult men and women.1 These deaths reflect nearly one third of deaths from all causes; many of which were largely preventable through lifestyle modifications. The theme of the 3rd Annual Building Healthy Lifestyles Conference was Modifying Lifestyles to Enhance Physical Activity, Diet, and Reduce Cardiovascular Disease. This article provides a summary and conclusion of the articles written as the conference proceedings.
In his article, McKeown2 introduced the term, epidemiologic transition, which describes changing patterns of population distributions in relation to changing patterns of mortality, fertility, life expectancy, and the leading causes of death. According to Omran3, originator of the concept, the key proposition of the epidemiologic transition is an occurrence of a long-term shift in mortality and disease patterns where pandemics of infection are gradually displaced by degenerative and man-made diseases as the chief form of morbidity and primary cause of death. According to the American Heart Association1, in 1900 nearly 27,000 deaths were attributed to coronary heart disease (CHD). This number increased steadily in the 20th century to an apex of 770,000 deaths in 1985. Since then, deaths from CHD have decreased to 446,000 deaths in 2005. The rise in CHD in the 20th century was coupled by declining mortality from infectious disease from the beginning to the end of the century. The value of tracking longitudinal data is it helps researchers to understand changing patterns of health and disease in populations and to identify interactive factors that modify the velocity of changes, such as demographic patterns, economic distributions and changes, social determinants and their related consequences.
McKeown2 further notes that the shift in the patterns of mortality over time is consistent with the three transitional phases that have occurred in the tracking of human life and related to trends in mortality. The first phase, the Age of Pestilence and Famine, is characterized by high and fluctuating mortality rates with variable life expectancy and low average life span. Here, the average life expectancy was about 30 years. The second phase, the Age of Receding Pandemics, is characterized by declining mortality rates, an increase in life expectancy with the introduction of chronic diseases as a cause of death. In this phase, life expectancy rose to 50 years. The third phase, the Age of Degenerative and Man-Made diseases, describes the condition in developed nations in the late 19th and 20th centuries. Here, societies are characterized by rapid advances in industrialization, mechanization, and computerization with the average life expectancy increasing to about 70 years. The changes described in each transitional phase reflect the complexity of the epidemiologic transition. In the third phase, increases in urban living with a consequent lower need for physical activity, changing food patterns and altered caloric composition, and changes in the social and cultural behavioral patterns collectively help to explain the rise in CHD during the latter part of the 20th century.
In examining the historical determinants attributed to the rise in CHD, Heath4 also noted public health advances in developed countries contributed to the decline in infectious diseases in the early 20th century, including improved sanitation of the environment for safer water delivery and sewage disposal and improvements in the general living and working environments of people. Advances in the use of antibiotics and vaccinations for epidemic illnesses and changes in personal behaviors of tobacco use, diet, alcohol consumption, and physical activity also contributed to the displacement of infectious disease for CHD as a leading cause of mortality. In an attempt to understand why chronic disease affects some people (e.g., African Americans) more than others, Heath4 noted it is unlikely that the rapid changes in society were sufficient to alter the basic genotype of humans. Instead, he speculated that the environmental changes have been sufficient to alter gene expressions in unhealthful ways to increase susceptibility for CHD.
In his review of the biological mechanisms for CHD, Leon5 noted that atherosclerosis and chronic inflammation of the arterial wall promotes endothelial cell injury in a manner that causes a cascade of changes to promote CHD. Endothelial cell injury permits lipid infiltration, oxidization of low density lipoproteins, resultant fibrocalcific plaque, and progressive coronary stenosis. Numerous factors can accelerate the atherosclerotic process including non-modifiable factors, such as genetics, aging, and gender differences, and modifiable physiologic and metabolic factors such as atherogenic dyslipidemia, hypertension, and diabetes mellitus. Lifestyle-related risk factors also have a strong potential to influence the development of atherosclerosis and include smoking, atherogenic dietary habits, physical inactivity, and associated reduced physical fitness, and overweight and obesity status.
As reflected by the theme of the Building Healthy Lifestyles Conference, modifying lifestyle risk factors is of primary importance to reduce CVD and in particular, CHD. In her paper, Johnston6 provides an overview of how dietary behaviors can modify the risk for CHD. Echoing Leon’s5 description of the role of arterial inflammation on the development of atherosclerosis, Johnston6 describes how pathogen invasion, including elevated blood cholesterol or glucose concentrations, cigarette smoke and pollutants, chemical solvents, obesity and stress, have the potential to damage vascular tissues through a series of immune-system mediated reactive inflammatory processes. Unless eliminated, these inflammatory mediators can chronically inflame the endothelium to cause permanent damage and clinical CHD outcomes. While several lifestyle behaviors can reduce the risks for chronic inflammation, such as smoking cessation, weight loss, physical activity, and stress management, dietary modifications have a powerful effect on reducing endothelial inflammation. The importance of diet on CHD was highlighted by Ygnve7, who provided examples from a number of groundbreaking studies, from ecological to randomized clinical trials, within the US and in Europe that showed scientific evidence to support the relationship between diet and CHD. Johnston6 discussed two diets (i.e., Mediterranean and vegetarian) and several functional foods known for their anti-inflammatory benefits in reducing CHD. The Mediterranean diet is high in fruits, vegetables, cereals, beans, nuts and seeds and olive oil. Red meat is rarely eaten and fish and dairy products are eaten sparingly. Similarly, the vegetarian diet is high in fruits, vegetables, and nuts that are high in antioxidant nutrients and polyphoenols, and low in foods containing arachidonic acid known to be a powerful precursor of endothelial inflammation. The types of foods included in the Mediterranean and vegetarian diets are collectively referred to as functional foods and are characterized as having high anti-inflammatory properties.
As we address dietary intake to reduce the incidence of CHD, Winham8 reminds us that we must be sensitive to the cultures and lifestyle experiences of persons in communities targeted for dietary interventions. When recommending dietary changes, one size does not fit all. Interventionists must be cognizant of the role of foods in different cultural groups and they must know if foods can be obtained, are affordable, and if they will be acceptable in taste and texture to the target population. It is also important to know if community members know how to prepare the recommended foods, if they are acceptable to religious and ethnic traditions (i.e., concepts of hot and cold foods in some Asian cultures), and how educational attainment may impact decisions to adopt health enhancing dietary behaviors.
Evidence is accumulating that poor sleep and chronic stress contribute to a chronic, inflammatory state that promotes atherosclerosis. Quan9 notes the value of sleep as a restorative process that allows the body to repair and restore itself from damage occurring during wakefulness. In particular, it appears that sleep is needed for changes to occur in the structure and organization of brain to retain and enhance memory and cognition. Sleep disturbances and duration of sleep are related to CHD. Obstructive sleep apnea, insomnia, restless leg syndrome, and parasomnias (sleep terrors, nightmares, and sleep walking) are also associated with an increased risk for CHD. Likewise, sleeping less than 7 hours or more than 10 hours per night increases the risks for CHD.
Davis10 showed evidence to support chronic stress, depression, and negative thinking as lifestyle-related risk factors for CVD. In a study of people who survived a heart attack, those with depression had a five year lower survival rate than those who were not depressed. Further, it appears that having negative emotions early in life increases one’s risk for CVD. In a retrospective evaluation of diaries kept by nuns during their early adulthood, those who had recorded negative emotions 60 years earlier showed a 2.5 increased risk of CVD mortality compared to nuns who had recorded positive emotions at the earlier date. What is the mechanism for this finding? A positive emotional state is related to less cardiovascular reactivity, endothelial inflammation, and cortisol levels, and fewer upper respiratory track infections. Davis10 provided seven suggestions for living a positive lifestyle: behaving as happy people do, engaging in enjoyable activities, sharing with others, lending help, taking nature breaks, being physically active, and increasing mindfulness of daily activities.
Leon5 also noted several lifestyle-related risk factors that can reduce CHD risk. As discussed by Carnethon11, physical inactivity was one of the 9 major contributors to heart disease mortality in the 2004 INTERHEART study, an international case-control study of risk factors for myocardial infarction. She cited data to show that physical inactivity is attributable to 12% of myocardial infarctions, second to hypertension (18%) and similar to type 2 diabetes mellitus (10%). The role of physical activity in the reduction of CHD has been studied since the 1940’s with evidence showing a consistent, dose response gradient between increased levels of physical activity and fitness and reductions in the CHD morbidity and mortality. In 2005 the US Centers for Disease Control (CDC) and the American College of Sports Medicine (ACSM) concluded that regular, moderate intensity physical activity was beneficial to reduce the risks for many chronic diseases, including CHD, and recommended adults accumulate at least 30 min/day of moderate intensity physical activity on most days of the week to reduce their chronic disease risks.12 In 2007, the ACSM and the American Heart Association updated the recommendations to clarify that a frequency of 5 days/week was a recommended frequency for activity and that combinations of moderate and vigorous intensity physical activity was optimal to reduce chronic disease risks.13 In her article, Carnethon addresses the question, how much physical activity is enough to reduce CHD risks? From available evidence, it appears that as little as 10 min/day of physical activity is sufficient to increase physical fitness, accumulating a week’s worth of physical activity in two days is equally effective in reducing mortality as spreading out activity over 5 or more days, and that achieving the recommended levels of physical activity can reduce the risks of mortality from CVD by nearly 30%.
If physical activity can significantly reduce the risks for CHD, why are nearly 40% of US adults inactive at health-enhancing levels?14 Heath4 attributes changes in social and demographic patterns in the last 40 years as causal factors in the reduction of regular physical activity. He cites a 10-fold increase in the use of automobiles, a decrease in time spent children spend in activity during physical education classes, and a reduction in the amount of physical activity required to one’s work, as well as the intensity of activities engaged in during non-work pursuits.
Systematic, evidence-based approaches are needed to increase physical activity in communities. Tudor-Locke15 describes the development of the First Step Program, a pedometer facilitated, theory-based behavior modification program designed to increase physical activity in healthy adults and in adults with type 2 diabetes. She showed how pedometer-based programs can be effective in promoting physical activity, citing a meta-analyses study of pedometer-based intervention studies lasting from 4 weeks to 1 year, with 1,800 to 4,500 steps taken daily as associated with modest amounts of weight loss (0.05 kg/week).
In her keynote address, Dunn16 highlighted the success of lifestyle-behavioral interventions to reduce risk factors for CHD. However, she cautioned that lifestyle interventions may be interpreted differently based on the number and type of risk factors addressed. A physical activity intervention may be focused on one behavior while a multiple risk factor intervention trial may have several goals for changing behaviors. Thus, the success of interventions depends largely on the goals of the program. There is strong evidence that lifestyle interventions are effective in increasing physical activity in controlled clinical settings, home settings, community-wide, and in programs delivered via the internet. Further, lifestyle interventions are especially effective in subpopulations that are habitually sedentary at the start of the studies. Thus, given the broad array of evidence that lifestyle interventions are effective in reducing CVD risks in a wide variety of settings and populations, Dunn16 concludes the challenge is now to understand how organizational, policy, and political barriers to build the needed capacity to implement and market evidence-based interventions to people most in need of CVD risk reduction.
The proceedings from the 3rd Annual Building Healthy Lifestyles Conference showed how changes in diet and physical activity behavior have changed over the years, largely due to industrialization and societal changes and this has coincided with increases in mortality and morbidity from CVD. While the biological cascade of inflammation and lipid infiltration is well understood in the etiology of CHD, evidence is growing in the effectiveness of lifestyle dietary and physical activity strategies to prevent inflammatory damage on arterial endothelial cells. It is becoming evident that emerging risk factors, such as getting an adequate amount of high quality sleep, having positive emotions, and reducing stress are important to reduce the risks for CHD. As a scientific community, we have come a long way in understanding how and why CHD occurs. Yet, we have more work ahead to translate scientific knowledge into community practice. We must never rest on our laurels in thinking we have left infectious diseases and the apex of CHD mortality rates in the past. McKeown2 reminds us about the changing patterns of mortality and population dynamics characterized by the epidemiologic transition. He indicates growing threat for chronic and infectious diseases in developing nations, with CHD rising in countries fueled by high poverty level, malnutrition, low educational attainment, and poor social organizations needed to combat the rise of CVD. As such, it is important to continue a focus on risk factor reduction in individuals and in communities, and as well, focus on environmental conditions and policies that can minimize the global impact CVD and its associated outcomes in all population groups.
In summary, the overall mission of the Building Healthy Lifestyles Conference series is to address lifestyle factors that have the potential to make a positive impact on chronic diseases and disabilities. In the third year, lifestyle factors as they relate to CVD were addressed. The conference mission is accomplished by providing a forum where scientific experts can come together with community practitioners to discuss strategies to optimize the translation of research into practice for the common goal of reducing the global burden that is attributable to CVD.
No conflict of interest was declared by the author. The authors were supported by National Heart, Lung, and Blood Institute (NIH-NHLBI, 1R13HL091657-01). The content is solely the responsibility of the author and does not necessarily represent the official views of the National Heart, Lung, and Blood Institute, or Arizona State University.