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In 2008, the American Heart Association (AHA) reported that an estimated one in three U.S. adults have one or more types of cardiovascular disease (CVD)1; a category of diseases which includes high blood pressure, coronary heart disease (CHD), heart failure, and stroke. The high prevalence, coupled with high costs that are associated with CVD, are factors that contribute to the current burden of CVD in the U.S. CVD is progressive in nature and many diagnosed individuals will present with symptoms or a clustering of risk factors. However, CVD is largely preventable and evidence-based research strongly supports the use of aggressive risk factor reduction, which includes the adoption and maintenance of healthy lifestyle practices throughout the lifespan, to decrease the burden associated with CVD.
The Building Healthy Lifestyles (BHL) conference series with the focus of Translating Research to Practice was initiated in 2005 to provide a regional forum for key stakeholders from research, higher education, public health and community programs to come together on an annual basis to discuss strategies for building healthy lifestyles. In 2008, the theme of the third annual BHL conference was Modifying Lifestyles to Enhance Physical Activity, Diet, and Reduce Cardiovascular Disease. The BHL conference was held on February 28, 29, and March 1, 2008 at Arizona State University at the Polytechnic campus in Mesa, AZ and had four specific objectives:
The keynote lecture was provided by Dr. Andrea Dunn, titled “The Effectiveness of Lifestyle Physical Activity Interventions to Reduce Cardiovascular Disease”2. This lecture provided an overview of physical activity lifestyle interventions designed to increase physical activity and reduce morbid conditions related to CVD.
Four related topic areas associated with CVD provided a framework for the conference program as depicted in Figure 1.
The first topic area dealt with the transitions in mortality, diet, and physical activity that have occurred over time. Causes for the increase in CVD are multifactoral and reflect long-term changes in cultural and societal norms, economic factors, technology, and lifestyle behaviors. The transition from infectious diseases to CVD as leading causes of death in the 20th Century is often referred to as the epidemiologic transition in mortality patterns3, 4. There is evidence to support that the human genome has remained largely unchanged since the Late Paleolithic era. And, from a genetic standpoint, modern humans are quite similar to their “hunter-gatherer” ancestors5. Since the advent of the agricultural revolution, humans have experienced dramatic environmental and cultural changes5–8, which has resulted in a shift in the pattern of morbidity and mortality from infectious to chronic causes. The epidemiological transition for CVD has occurred quite rapidly, within less than 100 years, suggesting behavioral changes in diet and physical activity are often cited as causal factors.
Changes in physical activity behaviors over time may be regarded as a physical activity transition. In order to survive, hunter-gatherers had to exert themselves on a daily basis in order to secure food, water, and shelter from the elements. Our Paleolithic ancestors walked or ran between 5 to 10 miles per day as they hunted and foraged for food. They also lifted, carried, climbed, and participated in any other activity that was necessary to secure sustenance and protection. The conveniences of today’s industrialized society, such as automobiles and elevators, have made physical activity optional. Thus, it appears the hunter-gatherer of the Late Paleolithic era has evolved into today’s couch potato seeing that the inhabitants of modern societies have adopted a predominantly sedentary lifestyle. Since humans are genetically predisposed to live a highly active lifestyle, deviation from that may have contributed to the rise in obesity rates and subsequent development of chronic diseases8.
Changes in technology, animal husbandry, agricultural practices over time have lead to a dietary transition. In the Paleolithic era, there was no single universal diet that was consumed by the hunter-gatherers. Instead, dietary patterns varied by factors such as geographic locale and climate5, 6. Prior to the development of agriculture and animal husbandry, dietary choices would have been limited to minimally processed, wild plant and animal foods6. The fundamental components of the hunter-gatherer diet included whole, natural, and fresh foods, such as fruits and vegetables. When compared to the average American diet, the Paleolithic diet contained 2 to 3 times more fiber, 4 times more ω-3 fats, 1.5 to 2.0 times more polyunsaturated and monounsaturated fats, and 60–70% less saturated fat. Protein intake in the hunter-gatherer was 2 to 3 times higher and sodium intake was 4 to 5 times lower8. Further, foods that are now considered dietary staples, such as dairy products, cereals, refined sugars, refined vegetable oils, and processed foods were not consumed during the Paleolithic Era5, 6. These discrepancies between the diet that we are genetically designed to eat and what we consume today have also contributed to the epidemiological transition towards chronic diseases, such as CVD6.
The second and third topic areas for the BHL conference framework are physical activity and diet; two powerful behavioral risk factors for CVD. Over the past few decades, evidence has accumulated on the role of physical activity in the prevention and treatment of CHD. Evidence-based research clearly suggests that individuals who participate in regular physical activity have a reduced risk of developing CHD9, 10. Furthermore, habitual physical activity has been suggested to reduce symptoms in individuals with pre-existing CVD10. Physiological adaptations to physical activity include an improvement in myocardial contraction, decreased resting heart rate, and increased stroke volume during rest and exercise11–13. Regular physical activity improves endothelial function and flow-mediated dilation and increases coronary collateral artery formation11–13 and reduces platelet aggregation11–13. Physical activity has both chronic and acute benefits14. The long-term benefits of physical activity include a reduction in atherosclerotic risk factors including elevated blood pressure, insulin resistance and glucose intolerance, elevated triglycerides, and low high-density lipoprotein cholesterol (HDL-C) levels. When combined with weight loss, physical activity can also improve low-density lipoprotein cholesterol (LDL-C) levels. There are also a number of acute cardiovascular benefits that result from recent activity; these include a reduction in triglycerides and systolic blood pressure and increase in HDL-C levels. Recent physical activity also improves insulin sensitivity and is beneficial for glucose homeostasis14.
It is well appreciated that diets low in saturated fat and cholesterol reduce blood cholesterol concentrations indirectly by protecting the vascular endothelium. Also, low sodium diets favorably affect blood pressure. Accordingly, low fat, low sodium diet strategies are promoted by the American Heart Association (the Diet and Lifestyle Recommendations)15 and by the federal government (the Dietary Guidelines for Americans) to prevent or manage CVD outcomes16. Additionally, recent research demonstrates that functional foods, such as fish, red wine, fruit, garlic, cocoa, and nuts, directly protect the endothelium and promote healthy blood vessels17. Thus dietary strategies for reducing risk for CVD should focus on diets low in saturated fats (including trans-fatty acids) and high in functional foods that directly improve endothelial health.
The forth topic area in the BHL conference framework relates to the lifestyle influences of sleep disturbances and chronic stress as causal factors for CVD. Sleep and sleep-related disorders are topics that are gaining popularity in the medical and research community as determinants of poor health. It is estimated that 30–45% of the U.S. population has had a sleep complaint at least once and another 10–15% suffer from chronic insomnia18. Further, it has been estimated that sleep disorders, sleep deprivation, and sleepiness affect 70 million American. Normal sleep exerts important influences on the cardiovascular system in healthy individuals, as well as in those with underlying medical conditions. Both acute sleep deprivation and accumulated sleep debt has been linked to chronic health conditions, including CVD19. Although there is limited evidence examining the physiological mechanisms underlying the relationship between sleep disorders and CVD, it has been suggested that chronic sleep restriction may increase sympathetic nervous system activity to the heart20 and may also contribute to impaired endothelium-dependent vasodilation21. Both acute and chronic sleep deprivation may activate inflammatory process, which may result in an increase in inflammatory marker levels22–26. Sleep deprivation may also be associated with metabolic disorders and glucose intolerance19, conditions that increase one’s risk for CVD.
Stress has also been implicated in the development and progression of CVD27. Stress can be defined as “a state of threatened homeostasis provoked by a psychological, environmental, or physiological stressor”28. It has been suggested that repeated episodes of acute and chronic stress, in a susceptible person, can promote CVD. Prolonged exposure to stress also stimulates the release of hormones such as cortisol and insulin, which increases appetite and cravings for sweet and/or fatty foods. The extra weight is primarily deposited centrally, which promotes central adiposity and the subsequent release of insulin and inflammatory markers. Physical activity may improve stress levels by mood enhancement through the release of neurotransmitters (e.g., dopamine and serotonin, and endorphins)29.
An overarching concern is the increased prevalence of CVD among racial and ethnic minority populations. During the past several decades, the U.S. population has become increasingly more diverse. Approximately 67% of the U.S. population is made up of non-Hispanic whites. Projection figures estimate that the proportion of non-Hispanic whites will decrease to 60% in 10 years and may be as low as 50% by the middle of the 21st century30. While the proportion of non-Hispanic whites in the U.S. are declining, rates in certain ethnic groups are rising. Hispanics are currently the largest and fastest growing ethnic group, representing approximately 15% of the U.S. population30. Despite the fact that a large segment of the U.S. population represents a minority group, disparities in health care currently exist. In the U.S. and other countries, CVD is the leading cause of mortality in all major racial and ethnic groups31, 32. One possible explanation for CVD related health disparities is that minority populations have been consistently under-represented in research studies. This under-representation in studies may be due in part to lack of trust and/or ineffective methods used during recruitment32. Although numerous studies have suggested that the risk factors that predict CVD in whites also predict disease in minority populations, the prevalence and magnitude of their influence in different sub-groups may vary32. Therefore, in order to appropriately impact CVD related morbidity and mortality in the U.S., both the diversity of the population and issues that are central to different ethnic and minority groups needs to be considered33.
The BHL conference proceedings presented in this special supplement issue of the American Journal of Lifestyle Medicine present an overview of the four topic areas that comprise the conference framework. In this issue, the first section focuses on the impact of transitions on CVD. Dr. Robert McKeown discusses the epidemiological transition as it relates to CVD34 and Dr. Gregory Heath discusses physical activity transitions35. The second section focuses on current evidence regarding the role of physical activity and diet on CVD. Dr. Arthur Leon provides an overview of mechanisms for the development of CVD36 and Dr. Agneta Yngve discuss the evolution of diet on CVD37. Dr. Carol Johnston presents the role of functional foods as protective modifiers of CVD38. The third section addresses the promotion of physical activity to prevent CVD. Dr. Mercedes Carnethon provides an evidence-based overview of the dose of physical activity associated with protection from CVD39 and Dr. Catrine Tudor-Locke provides a narrative review of a research focus to increase physical activity in adults40. The fourth section addresses lifestyle factors related to physical activity, diet, and CVD. Dr. Stuart Quan discusses the role of sleep and sleep disturbances on the development of CVD41 and Dr. Mary Davis shows how social and emotional resilience to stress can reduce CVD42. The last section focuses on reducing the impact of CVD in racial and ethnic minorities with a discussion by Dr. Donna Winham on culturally tailored foods43.
While not part of this supplement issue, the 2008 Building Healthy Lifestyles Conference offered workshops that were aimed at teaching participants skills for heart-healthy food preparation, stress reduction, and planning physical activity interventions. As with past years, the conference program also included a scientific poster session for graduate students and faculty to present their scientific research related to building healthy lifestyles.
CVD is the leading cause of mortality in the U.S. with multiple etiologies comprising several levels of influence. The 3rd annual Building Healthy Lifestyles conference program explored the historical evidence that advanced CVD to become the leading cause of death in the U.S. The conference also examined the current evidence regarding the impact of lifestyle behaviors that either prevent (i.e., healthy dietary practices and regular physical activity) or promote (i.e., stress and poor sleep habits) CVD. Finally, CVD has been shown to disproportionately affect ethnically diverse populations; therefore, the conference also focused on strategies that are used to reduce the burden of CVD.