Foundational Factors for Cardiovascular Disease: Behavior Change as a First-Line

Updated:Jul 15,2014

Foundational Factors for Cardiovascular Disease: Behavior Change as a First-Line Preventive Strategy

Disclosure: None of the authors have any conflicts to disclose
Pub Date: Wednesday, Nov. 27, 2013
Author: Barry A. Franklin, PhD; Jenna Brinks, MS; Harold Friedman, MD
Affiliations: Barry A. Franklin, Ph.D., Director, Preventive Cardiology and Cardiac Rehabilitation, William Beaumont Hospital, Royal Oak, Professor of Internal Medicine, Oakland University William Beaumont School of Medicine, Rochester, Michigan, Jenna Brinks, M.S., Manager, Preventive Cardiology and Cardiac Rehabilitation, William Beaumont Hospital, Royal Oak, Michigan, Harold Friedman, M.D., Medical Director, Preventive Cardiology and Cardiac Rehabilitation, William Beaumont Hospital, Royal Oak, Michigan.


Spring B, Ockene JK, Gidding SS, Mozaffarian D, Moore S, Rosal MC, Brown MD, Vafiadis D, Cohen DL, Burke LE, Lloyd-Jones D; on behalf of the American Heart Association Behavior Change Committee of the Council on Epidemiology and Prevention, Council on Lifestyle and Cardiometabolic Health, Council for High Blood Pressure Research, and Council on Cardiovascular and Stroke Nursing. Better population health through behavior change in adults: a call to action. Circulation. 2013: published online before print October 7, 2013, 10.1161/01.cir.0000435173.25936.e1.

Article Text

The just-published American Heart Association (AHA) Science Advisory by Spring et al.1 highlights the rationale for and important role of behavior change in achieving AHA’s 2020 goals, “to improve the cardiovascular health of all Americans by 20% while reducing deaths from cardiovascular diseases (CVD) and stroke by 20%.”  Key strategies involve progressing from poor to intermediate and from intermediate to ideal healthy lifestyle behaviors and cardiovascular biomarkers at the individual, population, and health care system level.  This commentary builds on the themes detailed herein, with specific reference to behavior-related antecedents of CVD, unhealthy lifestyle habits and population health, current (suboptimal) provider counseling practices, assessing patients’ readiness to change, and research-based interventions to improve patients’ behaviors (e.g., the 5 A’s, motivational interviewing, overcoming inertia with downscaled goals).

Numerous studies have now shown that acute myocardial infarctions (AMI) often evolve from mild-to-moderate coronary artery stenosis.2,3  Rupture of a vulnerable atherosclerotic plaque with thrombus formation is believed to represent the triggering mechanism.3  Fortunately, the plaque components responsible for vulnerability are amenable to intervention via intensive coronary risk factor modification.  This may occur by defusing triggers of arterial inflammation and improving endothelial function, or both, in the absence of overt anatomic plaque regression.4

Accordingly, the soft lipid-rich component appears to be more tractable, with greater potential to regress under intensive risk factor modification than the more voluminous calcium-collagenous component of atherosclerotic plaque.  Because the anti-inflammatory and/or endothelial function benefits of intensive risk factor modification may occur soon after the intervention, these mechanisms may account for the early reduction in clinical cardiac events observed in contemporary cholesterol lowering trials.5

Regardless of the precise mechanisms, it appears that intensive risk factor modification may stabilize plaques, leaving them less likely to rupture. Collectively, these findings suggest a new paradigm for preventing and managing coronary heart disease (CHD).6
Unhealthy Habits, Population Health, and Mortality: The Cardiovascular Disease Pyramid
Population health is influenced by modulators in five domains – genetic predisposition, social circumstances, environmental exposures, behavioral patterns, and access to quality health care.7  When it comes to reducing early deaths, medical care has a relatively minor role, potentially preventing 1 in 10 premature deaths.  Rather, the single greatest opportunity to improve health and reduce premature death lies in favorably modifying unhealthy behaviors, which account for approximately 40% of all deaths in the United States (U.S.).  The top two behavioral causes of premature death, obesity/physical inactivity and cigarette smoking, are a result of unhealthy dietary and lifestyle choices (Figure 1).8   These adverse health behaviors are most prevalent among the less fortunate, that is, those with low socioeconomic status, less education, and limited access to health care.  Because patients with chronic disease typically spend approximately 5000 hours each year independent of medical providers, it is critical to connect them with health-promoting resources in their immediate environment.9  Support can take the form of helping patients find and utilize school/university-based healthy lifestyle options, worksite wellness initiatives,10 community resources (e.g., park district or community center programs, healthy fast food restaurant options, walking paths, biking trails, recreation centers, farmers’ markets)11 and prevention-focused health care systems.12 

Preventing or favorably modifying traditional and nontraditional (emerging) risk factors through a combination of lifestyle interventions and pharmacological therapy, complemented by public policy  to enhance health outcomes, is now widely recognized as the cornerstone of initiatives aimed at the primordial, primary, and secondary prevention of CHD.13,14  Although patients, and the medical community, often focus on medications as a first-line strategy to stabilize or favorably modify traditional risk factors (e.g., obesity, hypertension, dyslipidemia, diabetes), these drugs do not address the root causes—that is, the most proximal risk factors for CHD, including poor dietary habits, physical inactivity, and cigarette smoking (Figure 2).13,14  Notably, these unhealthy lifestyle practices strongly influence not only blood pressure, lipid/lipoprotein levels, triglycerides, and glucose-insulin homeostasis, but also nontraditional risk factors such as endothelial function, oxidative stress, inflammation (e.g., C-reactive protein), thrombosis/coagulation, and other intermediary pathways (e.g., psychosocial stressors).13  Accordingly, as the importance of favorably modifying unhealthy behaviors becomes increasingly apparent,15-17 it’s time to change our emphasis from sick care to health care12 with a focus on prevention and the foundational causes of CVD. 

Poor Dietary Habits
The AHA’s Diet and Lifestyle Recommendations for CVD Risk Reduction suggest balancing energy intake and energy expenditure to achieve or maintain a healthy weight and selecting a diet that is rich in fish, vegetables and fruits, whole-grain, high-fiber food, and foods with reduced amounts of saturated fat, cholesterol, sugar, and salt.18  These recommendations were echoed in a recent report intended to provide a useful framework for health practitioners and policy makers to understand contemporary issues related to the effects of dietary habits on CVD.19

Another systematic review found strong evidence of a causal relationship for cardioprotective dietary practices, including vegetables, nuts, and “Mediterranean” eating patterns, and adverse effects of trans-fatty acids and foods with a high glycemic index.20  In a recent multicenter trial in Spain, participants who were at high cardiovascular risk and randomly assigned to a Mediterranean diet supplemented with extra-virgin olive oil or nuts demonstrated a reduced incidence (approximately 31%) of major cardiovascular events as compared with their control diet counterparts (advice to reduce dietary fat).21  Other recent studies have shown that decreasing red meat consumption or the adoption of a vegetarian diet are associated with a lower mortality risk.22,23  Contemporary analyses have also shown that even modest reductions in dietary salt can substantially decrease future cardiovascular events and associated medical costs.24  Although epidemiological studies, controlled interventional trials, and systematic reviews have demonstrated the cardioprotective effects of omega-3 fatty acid consumption, either from marine sources or via supplements,25-28 other recent analyses have reported no additional cardioprotective benefit from omega-3 fatty acid supplementation.29,30  Collectively, these findings and other recent reports31 suggest that favorably modifying unhealthy dietary practices can result in a substantial reduction in initial or recurrent cardiovascular events.

Physical Inactivity/Low Fitness
A widely cited systematic review and meta-analysis of 33 physical activity studies (n = 883,372 participants) reported risk reductions of 30% to 50% for cardiovascular mortality and of 20% to 50% for all-cause mortality.32  Numerous studies also suggest that increasing the level of cardiorespiratory fitness, expressed as metabolic equivalents (1 MET = 3.5 mL O2/kg/min), significantly reduces the risk of CVD and dramatically improves prognosis.33  In fact, the reductions in risk parallel those observed with increasing physical activity, but are essentially twice as great for aerobic capacity (cardiorespiratory fitness).34  Among men and women with and without CHD, each 1 MET increase in exercise capacity is associated with an approximately 15% reduction in cardiovascular mortality, which compares favorably with the survival benefit conferred by low-dose aspirin, statins, β-blockers, and angiotensin-converting enzyme inhibitors after AMI.35,36  Indeed, a recent meta-analysis comparing the effectiveness of exercise treatment versus drug interventions on mortality outcomes in the secondary prevention of CHD reported similar benefits.37

Numerous studies and pooled analyses, in persons with and without CHD, have shown that walking speed and distance are powerful predictors of mortality in middle-aged and older adults.38-40  Data from the Concord Health and Ageing in Men Project, a cohort study of 1705 healthy men aged 70 and over living in several inner city suburbs in Sydney, Australia, was used to clarify the walking pace that may be associated with a heightened mortality.  At baseline, walking speed was carefully measured at the usual pace, documenting the fastest time from two trials.  A natural walking speed of 2 miles per hour (mph) was most predictive of early mortality, while older men who walked at speeds greater than this were less likely to die during the 6-year follow up.  In fact, no men who initially walked at speeds ≥ 3 mph were among the 266 deaths reported.41  These findings support the hypothesis that faster walking speeds are associated with increased survival, as has been previously reported in coronary patients.42  The modest difference in walking speed associated with increased mortality and increased survival supports the notion that the primary beneficiaries of an exercise program are those at the bottom of the fitness/activity continuum.

To answer the question, “Should we be advising our patients to walk or run?,” researchers used a meta-analysis to evaluate the effect of physical activity at progressive intensities on all-cause mortality.43  The results showed a dose-response curve from sedentary subjects to those with low-to-moderate exercise intensities, with an only minor additional risk reduction with vigorous physical activity.  Collectively, these data suggest that habitually sedentary patients should be counseled to become more physically active and/or fit by starting an exercise program, increasing lifestyle activity, or both, so as to move them out of the least fit, least active, “high-risk” cohort (bottom 20%).44  Advocating regular brisk walking, before gradually advising the additional benefits of jogging or running, would be an appropriate approach for most inactive patients.45

Cigarette Smoking 
A landmark study of British physicians found that, on average, cigarette smokers die approximately 10 years earlier than nonsmokers.  For someone who has smoked since adulthood, cessation at age 50 decreased their risk by one-half.  Those who quit by age 30 had the same level of risk as a nonsmoker.46  Among post-MI patients with left ventricular dysfunction, smoking cessation is associated with a 40% lower all-cause mortality rate as compared with persistent smokers over an average follow-up of 42 months.47  Moreover, a recent report showed that weight gain following smoking cessation was not associated with a reduction in the benefits of quitting smoking on CVD outcomes.48

Unquestionably, cigarette smoking remains the most common cause of preventable death and disability in the U.S.  Although important strides have been made in tobacco control, the self-reported smoking rate varies considerably among population subsets, from 1% among U.S. physicians to > 30% in some blue collar workers.  The smoking prevalence among U.S. adults  (≥ 18 years of age) now hovers at 20%, more than 8 million people are sick or disabled as a result of tobacco use, and smoking kills an estimated 450,000 Americans each year.49  Even brief periods of passive smoke exposure can lead to acute vascular injury characterized by mobilization of dysfunctional endothelial progenitor cells with blocked nitric oxide production.50  Secondhand smoke was responsible for an estimated 603,000 deaths worldwide in 2004, and approximately 63% of those deaths were due to ischemic heart disease.51  One provocative report found that never-smokers increased their risk of CHD by 30% if they lived with a smoker.52 Reductions in acute cardiovascular event rates have also been reported in several large U.S. cities and countries that have banned smoking in public places.53,54  By assuming that the tobacco war has been won, we risk consigning millions of Americans to premature death. 

Risk Factors as Harbingers of Cardiovascular Disease: Debunking the 50% Misconception
A widely-cited review concluded that 75% to 90% of CHD incidence is explained by traditional risk factors.55  Moreover, Framingham Heart Study participants with optimal levels of cardiovascular risk factors and lifestyle behaviors at 50 years of age were at very low risk of ever developing CVD, 5% and 8% for men and women, respectively.56  Collectively, these data and other recent reports57,58 discount the longstanding claim that only 50% of the incidence of CHD in the population is attributable to traditional risk factors, and suggest that a more rigorous focus on these and the unhealthy behaviors that promote them has great potential to reduce the burden of atherosclerotic CHD (Figure 2).55,59  Although physicians have been increasingly urged to amplify efforts to favorably modify traditional risk factors in their patients,59 a large, international contemporary database reported that conventional cardiovascular risk factors are consistent, common, and remain largely undertreated and under-controlled in many regions of the world, including the U.S.60  Achieving increased CVD risk reduction and decreased mortality rates will, no doubt, involve embracing the research-based behavior change interventions outlined by Spring et al,1 as well as heightened ‘employee-responsibility’ via worksite wellness initiatives (e.g., participation in health screenings, ‘know your numbers’, desirable health metrics),10 and efforts to improve cardiovascular health at the community level.11

Advising Patients Regarding Behavior Change: Are We Doing Enough?
The Behavioral Risk Factor Surveillance System reported in 2000 that only 3% of 153,805 adults surveyed in the U.S. adhere to 4 of 4 healthy lifestyle characteristics, including not smoking cigarettes, maintaining a normal body mass index (18.5 to 24.9 kg/m2), consuming ≥ 5 servings of fruits and vegetables per day, and regular physical activity.  The adherence rate was lower in blacks than in whites at 1.4% and 3.3%, respectively.61  These healthy lifestyle percentages were even lower (0.5% of blacks and 2.1% of whites) in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) cohort, a national cohort of blacks and whites recruited between 2003 and 2007.62  According to a more recent report, a substantial percentage of patients receiving elective percutaneous coronary intervention for stable angina do not achieve lifestyle and risk factor goals and therefore remain at increased risk for recurrent cardiac events.63  Among a large sample of 7519 patients with a previous self-reported cardiac or stroke event from countries with varying income levels, 18.5% continued to smoke, only 35.1% undertook high levels of occupational or leisure-time physical activity (> 3000 MET-min/wk), and 39.0% were eating a healthy diet.  Thus, the prevalence of healthy lifestyle behaviors was low, but more so in poorer countries.64

Although physicians and allied health professionals have regular opportunities to counsel patients regarding their lifestyle habits and risk factors, many have little or no training in the specific skills sets required for health promotion, especially application of behavior change interventions.65  Moreover, most physician practices are already overstretched, reimbursement for patient counseling and education remains suboptimal, and use of the electronic medical record may further decrease face-to-face dialogue with patients.  Despite the well-established benefits of regular physical activity, weight reduction, and smoking cessation, less than half of all patients report being counseled about one or more of these risk-reduction strategies during their most recent physician office visit.66-70  Collectively, these and other relevant reports71 suggest that physicians and/or their support staff often miss opportunities to counsel patients regarding the need for substantive lifestyle modification.  Yet, numerous studies have now shown that brief (e.g., 3-5 minutes) physician intervention during an office visit can play a critical role in patient implementation and outcomes.72 

Assessing Patients’ Readiness to Change Behaviors
Facilitating lifestyle changes requires patient participation, knowledge, education, attitude, and motivation; however, tailoring messages on lifestyle counseling to patients’ individual readiness to change increases the likelihood of success.  The Transtheoretical Stages of Change Model includes 6 stages of any behavioral intervention process: precontemplation (patient is not thinking about making lifestyle changes); contemplation (patient is considering but is not yet ready to change); determination (patient has taken some behavioral steps and intends to take action in the next 30 days); action (patient begins to consistently demonstrate the new behavior for < 6 months); maintenance (patient has been in action for ≥ 6 months); and, relapse (patient returns to former [unhealthy] lifestyle habits).73  Patients should be evaluated for their stage of readiness before being counseled to change a specific behavior.  For example, physicians and other healthcare professionals should consider the issues outlined in Table 1 when assessing a patient’s readiness to embark on a weight loss intervention.74

Facilitating Behavior Change
The likelihood that patients will or will not engage in a particular lifestyle behavior is governed by a myriad of socioeconomic, attitudinal, and cultural factors, including their expectations of the benefits, costs, and consequences of that behavior.65  Lack of or a suboptimal social support system, social isolation, or financial difficulties are often cited as common barriers to achieving successful lifestyle behavior changes.75,76  Strategizing with the patient to identify realistic options to overcome these barriers, real or perceived, is integral to changing unhealthy behaviors.  Practitioners should anticipate patients declaring that they are too busy to make certain lifestyle changes (e.g., a structured exercise program).  Moreover, failure to address underlying psychosocial factors such as depression, anger, denial, chronic life stress, and personality traits – factors commonly clustered in patients with CVD – can be obstacles to a healthy lifestyle and directly promote CHD.75,76

More than 80% of adults currently have an established source of health care services, and this percentage is expected to appreciably increase with implementation of the Affordable Care Act.  This shift will enable vulnerable subsets of the population who are more often plagued by unhealthy lifestyle practices to seek medical evaluation and care, empowering providers with heightened opportunities to facilitate improvements in population health over time.1  The 5 A’s approach has been reported to produce significant improvements in a variety of health behaviors, including smoking cessation, dietary choices, and physical activity (Figure 3).77,78  Fortunately, progress has been made in that more providers now perform the first 2 A’s, that is, assess the risk behavior and advise behavior change.  On the other hand, it is the less frequently performed A’s (agree, assist, arrange), which require more time to implement and specific counseling skill sets to facilitate, that have the greatest impact on healthful behavior change.79,80  The core of effective counseling is a patient-centered approach, whereby providers work with patients, helping them to create and implement an ‘action plan’ to reach their self-stated goals, resulting from carefully crafted questions posed by the provider.81  Although most people believe that a single behavior change is preferred at any given time, embracing the notion that sequential changes can build on success, multiple simultaneous changes may be easier to adopt because they quickly yield perceptible benefits.82

Motivational Interviewing
Spring et al.1 highlight the important role of motivational interviewing as a form of talk therapy used by the health care provider during patient encounters to help encourage a behavioral transformation.83,84  To accomplish this, the clinician must convey understanding, acceptance, and interest in the patient as an individual.  The first step is to identify the patient’s readiness to change their behavior by using empathy to identify suboptimal lifestyle practices.  Getting patients to consciously recognize the circumstances or scenarios that contribute to these behaviors is critical.  The next step is getting the individual to understand and accept the need for change.  This may entail altering longstanding unhealthy behaviors that may be linked to stressful situations, psychosocial variables, work and/or home environments, inadequate education, economic factors, or combinations thereof.  Confrontations and arguments must be avoided at this time, and interviewers should strive to encourage the patient to hear themselves express why they want to (or should) change.85  This is most effective using specific questions directed at the patient about why they need to change this behavior.  More important, the patient needs to be allowed to speak and the provider should actively listen.  The next step is to help the patient overcome inertia and become independent and self-motivating, emphasizing that time is an ally to successful lifestyle modification.  Finally, patients should be counseled on handling resistance and dealing with recidivism.

Overcoming Inertia with Downscaled Goals
For many patients, setting initial goals for risk factors or lifestyle habits (e.g., body weight reduction, increasing physical activity) may be unrealistic and discouraging, especially if contemporary guideline recommendations are literally embraced.  For example, the patient whose height is 172.9 cm and weighs 137.3 kg might be advised to reduce his body weight to a “normal” range (i.e., 75.6 kg), since this represents a body mass index corresponding to 25 kg/m2.  A preferred approach may be to ask this patient for a realistic initial weight goal, and the associated timeline for its attainment.  Regardless of response, if it is less than his/her current weight, the provider would agree with and support the patient’s objective.  Similarly, rather than counseling the habitually sedentary patient to exercise for ≥ 30 minutes/day on most days of the week, as current guidelines suggest, consider  recommending 10-minute exercise bouts, 3 times per week, over the initial month of physical conditioning.  By overcoming inertia, many patients subsequently find themselves exceeding these modest goals.

The treatment of CHD has evolved from simple lifestyle modification in the mid-to-late 1960s, largely focused on early ambulation, exercise training, and a prudent diet, to an array of costly and palliative coronary revascularization procedures that fail to address the underlying causes: poor dietary habits, physical inactivity, and cigarette smoking.  However, contemporary studies now suggest that behavior change and multifactorial risk factor modification – especially smoking cessation and more intensive measures to control hyperlipidemia with diet, drugs, and exercise – may slow, halt, or even reverse (albeit modestly) the otherwise inexorable progression of atherosclerotic CHD.86,87  Other studies have now shown that combining dietary therapy with drug treatment is more effective than drug treatment alone in improving brachial artery flow-mediated vasodilation,88 in correcting dyslipidemia,89,90 in reducing ambulatory blood pressure,91 and in reducing the risk of acute coronary syndromes.92

Chiuve et al.15,16 demonstrated that a healthy lifestyle plays an important role in the primary prevention of CHD and risk of sudden cardiac death in middle-aged and older men and women, respectively, even among those taking medications for hypertension or hypercholesterolemia.  Moreover, systematic reviews now show that the mortality risk reductions associated with lifestyle changes in patients with CHD are similar to those reported for cardioprotective medications after AMI.37,93  Collectively, these findings and other recent data suggest that the effects of lifestyle change and combination drug therapy on cardiovascular risk reduction appear to be independent and additive.94-96

As cardiovascular health care providers, we need to become champions of achieving healthy lifestyle overhauls in our patients to prevent the development and progression of CVD.  Our younger patients should be regularly counseled to favorably modify unhealthy lifestyle habits, including poor dietary practices, physical inactivity, and cigarette smoking.  For patients aged 40 to 50 years, who already have ≥ 2 major risk factors, the elevated lifetime risks of developing CVD (69% for men and 50% for women) mandate adoption of adjunctive preventive therapies, including cardioprotective medications.56  Accordingly, patients should be directed to comprehensive programs designed to prevent or change unhealthy behaviors and facilitate cardiovascular risk reduction, including individually tailored interventions to circumvent or attenuate barriers to participation and adherence.  Achieving these goals will, no doubt, involve embracing the research-based behavior change interventions and health care system improvements outlined by Spring et al.1


  1. Spring B, Ockene JK, Gidding SS, et al.  Better population health through behavior change in adults: a call to action.  Circulation 2013, [Published online October 7]. DOI: 10.1161/01.cir.0000435173.25936.e1
  2. Little WC, Constantinescu M, Applegate RJ, et al.  Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease?  Circulation 1988;78(5, Pt 1):1157-1166.
  3. Falk E, Shah PK, Fuster V.  Coronary plaque disruption.  Circulation 1995;92(3):657-671.
  4. Pearson TA, Mensah GA, Alexander RW, et al.  Markers of inflammation and cardiovascular disease: application to clinical and public health practice---A statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association.  Circulation 2003;107(3):499-511.
  5. Nissen SE.  High-dose statins in acute coronary syndromes: not just lipid levels.  JAMA 2004;292(11):1365-1367.
  6. Franklin BA.  Coronary revascularization and medical management of coronary artery disease: changing paradigms and perceptions.  Eur J Cardiovasc Prev Rehabil 2006;13(5):669-673.
  7. Schroeder SA.  Shattuck Lecture. We can do better – improving the health of the American people.  N Engl J Med 2007;357(12):1221-1228.
  8. Mokdad AH, Marks JS, Stroup DF, Gerberding JL.  Actual causes of death in the United States, 2000.  JAMA 2004;291(10):1238-1245.
  9. Asch DA, Muller RW, Volpp KG.  Automated hovering in health care – watching over the 5000 hours.  N Engl J Med 2012;367(1):1-3.
  10. Carnethon M, Whitsel LP, Franklin BA, et al.  Worksite wellness programs for cardiovascular disease prevention: a policy statement from the American Heart Association.  Circulation 2009;120(17):1725-1741.
  11. Pearson TA, Palaniappan L, Artinian NT, et al.  American Heart Association Guide for improving cardiovascular health at the community level, 2013 update: a scientific statement for public health practitioners, healthcare providers, and health policy makers.  Circulation 2013;127(16):1730-1753.
  12. Fani Marvasti F, Stafford RS.  From sick care to health care – reengineering prevention into the U.S. system.  N Engl J Med 2012;367(10):889-891.
  13. Mozaffarian D, Wilson PWF, Kannel WB.  Beyond established and novel risk factors: lifestyle risk factors for cardiovascular disease.  Circulation 2008;117(23):3031-3038.
  14. Franklin BA, Cushman M.  Recent advances in preventive cardiology and lifestyle medicine; a themed series.  Circulation 2011;123(20):2274-2283.
  15. Chiuve SE, McCullough ML, Sacks FM, Rimm EB.  Healthy lifestyle factors in the primary prevention of coronary heart disease among men: benefits among users and nonusers of lipid-lowering and antihypertensive medications.  Circulation 2006;114(2):160-167.
  16. Chiuve SE, Fung TT, Rexrode KM, et al.  Adherence to a low-risk, healthy lifestyle and risk of sudden cardiac death among women.  JAMA 2011;306(1):62-69.
  17. de Waure C, Lauret GJ, Ricciardi W, et al.  Lifestyle interventions in patients with coronary heart disease: a systematic review.  Am J Prev Med 2013;45(2):207-216.
  18. Lichtenstein AH, Appel LJ, Brands M, et al.  Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee.  Circulation 2006;114(1):82-96.
  19. Mozaffarian D, Appel LJ, Van Horn L.  Components of a cardioprotective diet: new insights.  Circulation 2011;123(24):2870-2891.
  20. Mente A, de Koning L, Shannon HS, Anand SS.  A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease.  Arch Intern Med 2009;169(7):659-669.
  21. Estruch R, Ros E, Salas-Salvadó J, et al.  Primary prevention of cardiovascular disease with a Mediterranean diet.  N Engl J Med 2013;368(14):1279-1290.
  22. Pan A, Sun Q, Bernstein AM, et al.  Red meat consumption and mortality: results from 2 prospective cohort studies.  Arch Intern Med 2012;172(7):555-563.
  23. Crowe FL, Appleby PN, Travis RC, Key TJ.  Risk of hospitalization or death from ischemic heart disease among British vegetarians and nonvegetarians: Results from the EPIC-Oxford cohort study.  Am J Clin Nutr 2013;97(3):597-603.
  24. Coxson PG, Cook NR, Joffres M, et al.  Mortality benefits from US population-wide reduction in sodium: projections from 3 modeling approaches.  Hypertension 2013;61(3):564-570.
  25. Kris-Etherton PM, Harris WS, Appel LJ, AHA Nutrition Committee.  American Heart Association. Omega-3 fatty acids and cardiovascular disease: new recommendations from the American Heart Association.  Arterioscler Thromb Vasc Biol 2003;23(2):151-152.
  26. Wang C, Harris WS, Chung M, et al.  n-3 Fatty acids from fish or fish-oil supplements, but not α-linolenic acid, benefit cardiovascular disease outcomes in primary-and secondary-prevention studies: a systematic review.  Am J Clin Nutr 2006;84(1):5-17.
  27. Psota TL, Gebauer SK, Kris-Etherton P.  Dietary omega-3 fatty acid intake and cardiovascular risk.  Am J Cardiol 2006;98(Suppl 4A):3i-18i.
  28. Mozaffarian D, Lemaitre RN, King IB, et al.  Plasma phospholipid long-chain ω-3 fatty acids and total and cause-specific mortality in older adults.  Ann Intern Med 2013;158(7):515-525.
  29. Rizos EC, Ntzani EE, Bika E, et al.  Association between omega-3 fatty acid supplementation and risk of major cardiovascular disease events: a systematic review and meta-analysis.  JAMA 2012;308(10):1024-1033.
  30. Risk and Prevention Study Collaborative Group, Roncaglioni MC, Tombesi M, Avanzini F, et al.  n-3 fatty acids in patients with multiple cardiovascular risk factors.  N Engl J Med 2013;368(19):1800-1808.
  31. Dehghan M, Mente A, Teo KK, et al.  Relationship between healthy diet and risk of cardiovascular disease among patients on drug therapies for secondary prevention: a prospective cohort study of 31 546 high-risk individuals from 40 countries.  Circulation 2012;126(23):2705-2712.
  32. Nocon M, Hiemann T, Müller-Riemenschneider F, et al.  Association of physical activity with all-cause and cardiovascular mortality: a systematic review and meta-analysis.  Eur J Cardiovasc Prev Rehabil 2008;15(3):239-246.
  33. Kaminsky LA, Arena R, Beckie TM, et al.  The importance of cardiorespiratory fitness in the United States: the need for a national registry.  A Policy Statement from the American Heart Association.  Circulation 2013;127(5):652-662.
  34. Williams PT.  Physical fitness and activity as separate heart disease risk factors: a meta-analysis.  Med Sci Sports Exerc 2001;33(5):754-761.
  35. Kodama S, Saito K, Tanaka S, et al.  Cardiorespiratory fitness as a quantitative predictor of all-cause mortality and cardiovascular events in healthy men and women: a meta-analysis.  JAMA 2009;301(19):2024-235.
  36. Boden WE, Franklin BA, Wenger NK.  Physical activity and structured exercise for patients with stable ischemic heart disease.  JAMA 2013;309(2):143-144.
  37. Naci H, Ioannidis JPA.  Comparative effectiveness of exercise and drug interventions on mortality outcomes: metaepidemiological study.  BMJ 2013;347:f5577 doi: 10.1136/bmj.f5577 (Published 1 October 2013).
  38. Hakim AA, Petrovitch H, Burchfiel CM, et al.  Effects of walking on mortality among nonsmoking retired men.  N Engl J Med 1998;338(2):94-99.
  39. Kavanagh T, Hamm LF, Beyene J, et al.  Usefulness of improvement in walking distance versus peak oxygen uptake in predicting prognosis after myocardial infarction and/or coronary artery bypass grafting in men.  Am J Cardiol 2009;101(10):1423-1427.
  40. Studenski S, Perera S, Patel K, et al.  Gait speed and survival in older adults.  JAMA 2011;305(1):50-58.
  41. Stanaway FF, Gnjidic D, Blyth FM, et al.  How fast does the Grim Reaper walk?  Receiver operating characteristics curve analysis in healthy men aged 70 and over.  BMJ 2011;343:d7679 doi: 10.1136/bmj.d7679 (Published 15 December 2011).
  42. Beatty AL, Schiller NB, Whooley MA.  Six-minute walk test as a prognostic tool in stable coronary heart disease: Data from the Heart and Soul Study.  Arch Intern Med 2012;172(14):1096-1102.
  43. Löllgen H, Böckenhoff A, Knapp G.  Physical activity and all-cause mortality: An updated meta-analysis with different intensity categories.  Int J Sports Med 2009;30(3):213-224.
  44. Franklin BA, Lavie CJ, Squires RW, Milani RV.  Exercise-based cardiac rehabilitation and improvements in cardiorespiratory fitness: Implications regarding patient benefit.  Mayo Clin Proc 2013;88(5):431-437.
  45. Rankin AJ, Rankin AC, MacIntyre P, Hillis WS.  Walk or run? Is high-intensity exercise more effective than moderate-intensity exercise at reducing cardiovascular risk?  Scot Med J 2012;57(2)99-102.
  46. Doll R, Peto R, Boreham J, Sutherland I.  Mortality in relation to smoking: 50 years’ observations on male British doctors.  BMJ 2004;328(7455):1519-1527, doi: 10.1136/bmj.38142.554479.AE (published 22 June 2004).
  47. Shah AM, Pfeffer MA, Hartley LH, et al.  Risk of all-cause mortality, recurrent myocardial infarction, and heart failure hospitalization associated with smoking status following myocardial infarction with left ventricular dysfunction.  Am J Cardiol 2010;106(7):911-916.
  48. Clair C, Rigotti NA, Porneala B, et al.  Association of smoking cessation and weight change with cardiovascular disease among adults with and without diabetes.  JAMA 2013;309(10):1014-1021.
  49. Schroeder SA, Warner KE.  Don’t forget tobacco.  N Engl J Med 2010;363(3):201-204.
  50. Heiss C. Amabile N, Lee AC, et al.  Brief secondhand smoke exposure depresses endothelial progenitor cells activity and endothelial function: sustained vascular injury and blunted nitric oxide production.  J Am Coll Cardiol 2008;51(18):1760-1771.
  51. Öberg M, Jaakkola MS, Woodward A, et al.  Worldwide burden of disease from exposure to second-hand smoke: A retrospective analysis of data from 192 countries.  Lancet 2011;377(9760)139-146.
  52. Barnoya J, Glantz SA.  Cardiovascular effects of secondhand smoke: nearly as large as smoking.  Circulation 2005;111(20):2684-2698.
  53. Pell JP, Haw S, Cobbe S, et al.  Smoke-free legislation and hospitalizations for acute coronary syndrome.  N Engl J Med 2008;359(5):482-491.
  54. Glantz SA, Gibbs E.  Changes in ambulance calls after implementation of a smoke-free law and its extension to casinos.  Circulation 2013;128(8):811-813.
  55. Kannel WB, Vasan RS.  Adverse consequences of the 50% misconception.  Am J Cardiol 2009;103(3):426-427.
  56. Lloyd-Jones DM, Leip EP, Larson MG, et al.  Prediction of lifetime risk for cardiovascular disease by risk factor burden at 50 years of age.  Circulation 2006;113(6):791-798.
  57. Greenland P, Knoll MD, Stamler J, et al.  Major risk factors as antecedents of fatal and nonfatal coronary heart disease events.  JAMA 2003;290(7):891-897.
  58. Knot UN, Khot MB, Bajzer CT, et al.  Prevalence of conventional risk factors in patients with coronary heart disease.  JAMA 2003;290(7):898-904.
  59. Canto JG, Iskandrian AE.  Major risk factors for cardiovascular disease: Debunking the “only 50%” myth.  JAMA 2003;290(7):947-949.
  60. Bhatt DL, Steg PG, Ohman EM, et al.  International prevalence, recognition, and treatment of cardiovascular risk factors in outpatients with atherothrombosis.  JAMA 2006;295(2):180-189.
  61. Reeves MJ, Rafferty AP.  Healthy lifestyle characteristics among adults in the United States, 2000.  Arch Intern Med 2005;165(8):854-857.
  62. Ard J, Butsch S, Howard VJ, et al.  The national prevalence of healthy lifestyles is low and varies by race and geographic region.  Circulation 2007;115(8):e280 (Abstract).
  63. Khattab AA, Knecht M, Meier B, et al.  Persistence of uncontrolled cardiovascular risk factors in patients treated with percutaneous interventions for stable coronary artery disease not receiving cardiac rehabilitation.  Eur J Prev Cardiol 2013;20(5):743-749.
  64. Teo K, Lear S, Islam S, et al.  Prevalence of a healthy lifestyle among individuals with cardiovascular disease in high-, middle-, and low-income countries: The Prospective Urban Rural Epidemiology (PURE) study.  JAMA 2013;309(15):1613-1621.
  65. Franklin BA, Vanhecke TE.  Counseling patients to make cardioprotective lifestyle changes: Strategies for success.  Preventive Cardiology 2008 Winter;11(1):50-55.
  66. Wee CC, McCarthy EP, Davis RB, Phillips RS.  Physician counseling about exercise.  JAMA 1999;282(16):1583-1588.
  67. Galuska DA, Will JC, Serdula MK, Ford ES.  Are health care professionals advising obese patients to lose weight?  JAMA 1999;282(16):1576-1578.
  68. Stafford RS, Farhat JH, Misra B, Schoenfeld DA.  National patterns of physician activities related to obesity management.  Arch Fam Med 2000;9(7):631-638.
  69. Doescher MP, Saver BG.  Physicians’ advice to quit smoking.  The glass remains half empty.  J Fam Pract 2000;49(6):543-547.
  70. Ma J, Urizar GG Jr, Alehegn T, Stafford RS.  Diet and physical activity counseling during ambulatory care visits in the United States.  Prev Med 2004;39(4):815-822.
  71. Quinn VP, Stevens VJ, Hollis JF, et al.  Tobacco-cessation services and patient satisfaction in nine nonprofit HMOs. Am J Prev Med 2005;29(2):77-84.
  72. Albright CL, Cohen S, Gibbons L, et al.  Incorporating physical activity advice into primary care: Physician-delivered advice within the activity counseling trial.  Am J Prev Med 2000;18(3):225-234.
  73. Prochaska JO, DiClemente CC.  Transtheoretical therapy: Toward a more integrative model of change.  Psychother Theory Res Pract 1982;19(3):276-288.
  74. The practical guide: Identification, evaluation, and treatment of overweight and obesity in adults.  Bethesda, Md.: National Institutes of Health; National Heart, Lung, and Blood Institute, NHLBI Obesity Education Initiative, North American Association for the Study of Obesity, 2000. NIH publication no. 00-4084.
  75. Rozanski A, Blumenthal JA, Kaplan J.  Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy.  Circulation 1999;99(16):2192-2217.
  76. Williams RB, Barefoot JC, Schneiderman N.  Psychosocial risk factors for cardiovascular disease: More than one culprit at work.  JAMA 2003;290(16):2190-2192.
  77. Chase EC, McMenamin SB, Halpin HA.  Medicaid provider delivery of the 5A’s for smoking cessation counseling.  Nicotine Tob Res 2007;9(11):1095-1101.
  78. Alexander SC, Cox Me, Boling Turer CL, et al.  Do the five A’s work when physicians counsel about weight loss?  Fam Med 2011;43(3):179-184.
  79. Forman-Hoffman V, Little A, Wahls T.  Barriers to obesity management: A pilot study of primary care clinicians.  BMC Fam Pract 2006;7:35. DOI:10.1186/1471-2296-7-35.
  80. Ruelaz AR, Diefenbach P, Simon B, et al.  Perceived barriers to weight management in primary care?perspectives of patients and providers.  J Gen Intern Med 2007;22(4):518-522.
  81. Epstein RM, Franks P, Fiscella, et al.  Measuring patient-centered communication in patient-physician consultations: Theoretical and practical issues.  Soc Sci Med 2005;61(7):1516-1528.
  82. Hyman DJ, Pavlik VN, Taylor WC, Goodrick GK, Moye L.  Simultaneous vs sequential counseling for multiple behavior change.  Arch Intern Med 2007;167(11):1152-1158.
  83. Bundy C.  Changing behavior: Using motivational interviewing techniques.  J R Soc Med 2004;97(Suppl 44):43-47.
  84. Britt E, Hudson SM, Blampied NM.  Motivational interviewing in health settings: A review.  Patient Educ Couns 2004;53(2):147-155.
  85. Verheijden MW, Bakx JC, Delemarre IC, et al.  GPs’ assessment of patients’ readiness to change diet, activity and smoking.  Br J Gen Pract 2005;55(515):452-457.
  86. Superko HR, Krauss RM.  Coronary artery disease regression.  Convincing evidence for the benefit of aggressive lipoprotein management.  Circulation 1994;90(2):1056-1069.
  87. Roberts WC.  Preventing and arresting coronary atherosclerosis.  Am Heart J 1995;130(3, Pt 1):580-600.
  88. Søndergaard E, Møller JE, Egstrup K.  Effect of dietary intervention and lipid-lowering treatment on brachial vasoreactivity in patients with ischemic heart disease and hypercholesterolemia.  Am Heart J 2003;145(5):E19.  DOI:10.1016/S0002-8703(03)00078-4.
  89. Barnard RJ, DiLauro SC, Inkeles SB.  Effects of intensive diet and exercise intervention in patients taking cholesterol-lowering drugs.  Am J Cardiol 1997;79(8):1112-1114.
  90. Chan DC, Watts GF, Mori TA, et al.  Factorial study of the effects of atorvastatin and fish oil on dyslipidaemia in visceral obesity.  Eur J Clin Invest 2002;32(6):429-436.
  91. Conlin PR, Erlinger TP, Bohannon A, et al.  The DASH diet enhances the blood pressure response to losartan in hypertensive patients.  Am J Hypertens 2003;16(5, Pt 1):337-342.
  92. Pitsavos C, Panagiotakos DB, Chrysohoou C, et al.  The effect of Mediterranean diet on the risk of the development of acute coronary syndromes in hypercholesterolemic people: A case-control study (CARDIO2000).  Coron Artery Dis 2002;13(5):295-300.
  93. Iestra JA, Kromhout D, van der Schouw YT, et al.  Effect size estimates of lifestyle and dietary changes on all-cause mortality in coronary artery disease patients: A systematic review. Circulation 2005;112(6):924-934.
  94. Sdringola S, Nakagawa K, Nakagawa Y, et al.  Combined intense lifestyle and pharmacologic lipid treatment further reduce coronary events and myocardial perfusion abnormalities compared with usual-care cholesterol-lowering drugs in coronary artery disease.  J Am Coll Cardiol 2003;41(2):263-272.
  95. Parmley WW.  In the statin era, how important are intense lifestyle changes?  J Am Coll Cardiol 2003;41(2):273-274.
  96. Franklin BA, Kahn JK, Gordon NF, Bonow RO.  A cardioprotective “polypill”?  Independent and additive benefits of lifestyle modification.  Am J Cardiol 2004;94(2):162-166.


Figure 1.  Numbers of U.S. deaths from behavioral causes, 2000.  The top two behavioral causes of premature death are cigarette smoking and obesity/physical inactivity, respectively, totaling more than 800,000 deaths.  Other behavioral causes include sexually transmitted diseases, alcohol, firearm, and drug-related deaths, and motor vehicle fatalities.  Source: Mokdad et al.8

Figure 2.  The evolutionary CVD pyramid.  Unhealthy lifestyle practices lead to risk factors, the progression of CVD, and, ultimately, adverse outcomes or clinical endpoints.  Prevention can be divided into 3 types: primordial (prevention of risk factors); primary (treatment of risk factors); and secondary (prevention of recurrent cardiovascular events), which can be modulated by environmental (e.g., air pollution) and psychosocial stressors, lifestyle change, and cardioprotective medications, if appropriate.  The first-line strategy to prevent initial or recurrent cardiac events is to favorably modify unhealthy lifestyle habits or practices, including poor dietary habits, physical inactivity, and cigarette smoking.  CVD signifies cardiovascular disease; MI indicates myocardial infarction; CHF, congestive heart failure; and PAD, peripheral arterial disease.  Sources: Mozaffarian et al and Franklin et al.13,14

Figure 3.  The 5 A’s to facilitate effective health behavior change counseling during a medical visit.  Although more providers now perform the first 2 A’s, that is, assess the risk behavior and advise behavior change, it is the latter, less frequently performed 3 A’s (shaded) that have the greatest impact on healthful behavior change.  Effective clinician behavior change strategies include using motivational interviewing along with rewards or incentives, asking patients to self-monitor behaviors, enhancing patients’ self-efficacy (confidence), accessing social support from family and friends, and scheduling regular follow-up communications/meetings to assess progress. Sources: Chase et al and Alexander et al.77,78.

Franklin Commentary - Figure 1
Figure 1.

Franklin Commentary - Figure 2
Figure 2.

Franklin Commentary - Figure 3
Figure 3.

Table 1. Brief Behavior Assessment of a Patient’s Weight Loss Initiative

Has patient sought weight loss on his/her own initiative?

Before initiating treatment, professionals must determine if patient recognizes the need for and benefits of weight loss and wants to lose weight.

What events have led patient to seek weight loss now?

Weight loss motivation and goals are evident by responses to this question.

What is patient’s level of stress or depression?

Patients who report higher-than-usual stress levels or depression may be unable to focus on weight management.
To increase the likelihood of weight-loss success, counseling may need to be initiated.

Does patient have an eating disorder?

Approximately 20% to 30% of obese patients who seek weight reduction (at university clinics) indulge in binge eating.
Binge eaters are typically distressed by their chaotic eating patterns; the greater the person’s distress or depression, the greater the need for additional forms of counseling (psychologic or nutritional).

Does patient understand the treatment requirements and believe that they can be met?

Health care professional and patient should select a course of treatment requirements together.
Treatment activities should include those that are a high priority for the patient and those that the patient believes can be achieved.

How much weight does the patient expect to lose?

Professionals must assist patients in understanding that slow, modest weight loss can improve health.

What other benefits does the patient anticipate?

In addition to weight loss, progress should be assessed by achievement of selected health improvement metrics, including increased physical activity or fitness.

Source: National Institutes of Health; National Heart, Lung, and Blood Institute, NHLBI Obesity Education Initiative, North American Association for the Study of Obesity, 2000.74

-- The opinions expressed in this commentary are not necessarily those of the editors or of the American Heart Association -- 

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