Our industrialized world presents numerous opportunities to indulge. Humans wrestle with increased levels of saturated fat and salt, decreased levels of fiber and exercise, widespread use of alcohol and tobacco, and higher consumption of calorically dense food. These factors, when combined, result in a mismatch between the genes carried forward from our evolutionary past and the new environment we have “suddenly” created. This has wreaked havoc with our biochemistry and physiology, which are fine-tuned for life conditions that existed more than 10,000 years ago (Cordain et al. 2005). There seems to be a disconnection between the patterns of nutrient intake and physical activity of our hunter-gatherer ancestors and those of modern, industrialized societies. This gap may serve as a clue to the global epidemic of chronic illnesses such as cardiovascular disease (CVD).
Although the prevalence of CVD-related deaths has declined since the 1980s, it remains the leading cause of mortality in the United States (American Heart Association [AHA] 2008). In 2003 CVD claimed 870,000 lives—over half attributed to coronary artery disease (CAD) (AHA 2008). In 2000 it was estimated that physical inactivity and poor diet contributed to 400,000 premature deaths (only tobacco use ranked higher). Data reveal that inactive people are twice as likely to develop CAD compared with active people (Roberts & Barnard 2005).
A deadly paradox exists between the public’s knowledge of health benefits from eating well and exercising and the number of people who actually partake in such a lifestyle. This is called a “health behavior gap.” It is imperative for individuals to live active, healthy lifestyles in their earlier years to avoid developing CAD risk factors later in life, but what if we reach middle age and have multiple risk factors? Are we able to reverse CAD and make up for the “health sins” we committed in our earlier years? This article addresses the likelihood of CAD regression and reversal and explores the importance of primary prevention in youth.
Although the pathophysiology of CAD is complex and multifactorial, the etiology can be attributed to endothelial dysfunction. Until recently, the inner lining (endothelium) of coronary arteries was thought to have little bearing on physiological function. However, scientists now recognize that the endothelial wall plays a vital role in vascular health. Endothelial dysfunction, the abnormal or impaired physiological function of the biochemical processes carried out by endothelial cells lining the inner surface of artery walls, can be attributed to smoking, elevated low-density lipoprotein (LDL) cholesterol, elevated blood glucose and inflammation. Endothelial dysfunction occurs early in the atherosclerosis process, contributes to disease development and progression, and can trigger acute cardiovascular events (Van Guilder et al. 2007).
Can atherosclerosis and endothelial dysfunction be reversed? Several investigations involving therapeutic lifestyle changes in CAD patients have demonstrated stabilization and reversal of the disease process, as well as improved endothelial function. Because low high-density lipoprotein (HDL) cholesterol values represent a strong independent risk factor for CVD, increased concentrations of HDL positively modify the process of atherosclerosis and endothelial dysfunction through several mechanisms. HDL cholesterol reverses cholesterol transport, removing cholesterol from the arterial wall. Additionally, HDL has been shown to prevent and correct endothelial dysfunction by facilitating vascular relaxation. It does this by increasing nitric oxide (a potent vasodilator) production, inhibiting blood cell adhesion to vascular endothelium and reducing platelet aggregability and coagulation (Calabresi, Gomaraschi & Franceschini 2003).
HDL cholesterol concentrations can be favorably improved with regular physical activity, and there appears to be a dose-
response relationship between weekly volume and the magnitude of improvement. In a review on lipid and lipoprotein adaptations to exercise, Durstine and others (2001) identified a caloric threshold range of 1,200–2,200 kilocalories per week (kcal/week), or the equivalent of 15–20 miles/week of brisk walking or jogging, as the expenditure required to elicit positive changes in the lipid profile. These energy expenditure values are associated with an average 2–8 milligrams per deciliter (mg/dl) increase in HDL cholesterol for each 1 mg/dl increase in HDL, corresponding to a 2%–3% reduction in mortality risk from CVD (Leon & Sanchez 2001). Regular physical activity also benefits cardiorespiratory fitness, which recently has been suggested as the ultimate marker for health outcomes and risk stratification (Franklin 2007). Swain and Franklin (2006) highlight that for each increase of 1 MET,
or 3.5 milliliters per kilogram of body weight per minute (ml/kg/min), in cardiorespiratory fitness there is a corresponding 8%–17% reduction in CVD and all causes of mortality. These same authors conclude that vigorous physical activity appears to be more cardioprotective than moderate physical activity.
Hambrecht and colleagues (1993) performed a classic study concerning the prospects of stopping or reversing CAD progression. To maximize the potential for CAD stabilization and/or regression, individuals focused on achieving a total weekly energy volume through physical activity of 1,500 and 2,200 kcal/week, respectively. Interestingly, individuals who expended 1,000 kcal/week or less experienced CAD progression. Because minimal energy expenditure guidelines from the American College of Sports Medicine and the Centers for Disease Control and Prevention are 1,000 kcal/week (American College of Sports Medicine [ACSM] 2006), the recommendations may need to be raised if there is going to be a positive modification to the global and international CAD epidemic.
The Lifestyle Heart Trial examined CAD patients who made widespread lifestyle adjustments and how these changes impacted the progression of atherosclerosis without lipid-lowering medications (Ornish et al. 1998). A total of 48 participants with moderate to severe CAD were divided into a usual-care group (following advice of personal physician) and an experimental group (10%-fat vegetarian diet, moderate aerobic exercise, stress management training, smoking cessation and group psychosocial support). Participants followed up 5 years later with an angiogram. Individuals in the experimental group experienced a regression in their CAD compared with the control group, in which researchers observed CAD progression. Additionally, there were twice as many cardiac events in the control group versus the experimental group over the 5-year period.
The previous section dealt with CAD reversal in individuals who have been positively diagnosed with disease. Preventing CAD development is the wiser choice, rather than waiting and trying to reverse it later, right? So, let’s talk about those who exhibit risk factors early in life (teens, 20s or 30s). Are they destined to develop significant CAD (morbidity) later? Can we significantly decrease our risk of death (mortality) from CAD if we maintain a favorable risk factor profile later, in our 30s, 40s and 50s?
It is well established that some CAD risk factors (high cholesterol, high blood pressure and elevated blood glucose) have the potential to sneak up without warning on people who do not receive regular screenings or do not possess adequate knowledge of these risk factors. As an aside, the adage that “you first have to admit you have a problem before you can fix it” certainly applies here. Recently, researchers demonstrated that healthy, young adults (18–30 years of age) had a poor understanding of modifiable risk factors for CVD (Lynch et al. 2006). More troubling is that fewer than 35% of this group recognized obesity as a risk factor for disease. On the 10-year follow-up, knowledge of risk factors did not impact risk factor levels in subjects. This study suggests that improving risk factor profiles goes beyond having appropriate knowledge, although it provides evidence for a continuing “health behavior gap” among the U.S. population. This phenomenon could certainly impact CAD morbidity and mortality in later years, as the development of these risk factors
begins in early life.
The central question is “What is the impact of early risk factor development on health in later years?” Recent data suggest that the presence of one or more major risk factors is positively linked to 90% or more of all CAD cases, therefore underlining primary prevention as early in life as possible. Daviglus and others (2004) assessed the relationship between risk factor profile in women and long-term CAD mortality risk over an average follow-up of 31 years. According to the results, a low risk factor profile (blood pressure < 120/80 millimeters of mercury [mm Hg], total cholesterol < 200 mg/dl, body mass index [BMI] < 25, no diabetes and no smoking) in young adulthood (age 18–39 years) was associated with a lower CAD mortality risk (0.7 deaths per 10,000 person-years) compared with two or more risk factors (5.4 deaths per 10,000 person-years). This study suggests that it is still more important to get “started off on the right foot” with risk factors earlier in life. Interestingly, only 20% of subjects (1,469 out of 7,302) were considered “low risk,” which is very similar to current numbers in the U.S. population (range of 3%–20%) (Daviglus et al. 2004).
Stamler and colleagues (2000) employed similar outcome measures as Daviglus and others (2004) in a study focused on long-term CAD mortality risk in younger men with normal and elevated levels of blood cholesterol. Results demonstrated a 2.15–3.63 times greater mortality risk with elevated cholesterol levels (>240 mg/dl) compared with favorable levels (<200 mg/dl) in young adulthood. In addition, the life expectancy of men with favorable cholesterol levels was 3.8–8.7 years longer.
This section gets closer to the “heart” of the matter: Can we
essentially make up for the poor health choices of our early years later in life? There will never be a better substitute than primary prevention (absence of risk factors) for lowering overall CAD mortality risk, as Stamler and colleagues reported in 1999. In findings similar to those of Daviglus and others (2004), subjects who were free of CAD risk factors had a 77%–92% reduction in mortality risk compared with those who had one or more risk factors. Interestingly, younger and middle-age subjects free of CAD risk factors had significantly greater life expectancies (~5.8–9.5 years), underscoring the importance of reaching middle age free of risk factors. Other researchers have delved further into the benefits of reaching middle age with a favorable risk factor profile. Two recent studies by Lloyd-Jones and colleagues clearly demonstrate the positive association between lower CVD (of which CAD is a part), mortality risk and favorable risk factor profiles by age 50 or “middle age.”
In the first study (Lloyd-Jones et al. 2006), researchers estimated lifetime risk of CVD mortality in men and women free of CVD at age 50 up to age 95. Subjects were stratified into groups based on risk factor profile (optimal, one or more not optimal, one or more elevated, one major risk factor, and two or more
major risk factors). Individuals with optimal risk profiles had a significantly lower lifetime risk of CVD (5.2% for men, 8.2% for women) compared with those who had two or more risk factors (68.9% for men, 50.2% for women). Also, low-risk men and women outlived their counterparts who had two or more risk factors by a median of >11 years and >8 years, respectively. In addition, presence of diabetes at age 50 was associated with the highest lifetime risk for CVD compared with other risk factors (67.1% for men, 57.3% for women).
The second study (Lloyd-Jones et al. 2007) offered estimates for lifetime risk of CVD mortality up to age 85 in men and women free of CVD between ages 40 and 59. Subjects were stratified into groups based on risk factor profile (optimal, zero elevated but one or more not optimal, one elevated, two elevated, and three or more elevated). Individuals with optimal risk factor profiles had a significantly lower lifetime risk of CVD (20.5% for men, 6.7% for women) compared with those who had three or more risk factors (35.2% for men, 31.9% for women). Also, low-risk men and women outlived their counterparts who had three or more risk factors by a median of >9 years and >7 years, respectively. Overall, both studies suggest that reaching middle age close to optimal risk profile is of utmost importance; therefore, intensive lifestyle changes should occur in younger ages to get to this point.
Another question being addressed in research is “Wouldn’t increasing longevity lead to larger numbers of sick and disabled older adults with poorer quality of life?” You wouldn’t draw that conclusion according to findings by Daviglus, Lloyd-Jones & Pirvada (2006). These researchers looked at middle-aged adults with varied risk profiles and followed them into old age. Adults who had low risk factors in middle age demonstrated a significantly higher quality of life in older ages compared with those who had three or more risk factors. The authors stated that a “clear gradient for health status” exists in older adults (risk factors increase, quality of life decreases), which underscores a major benefit for preventing the development of higher risk factor levels as one ages.
Is it possible to make up for the “sins” of one’s younger years? Through intensive lifestyle modification (diet, exercise, stress management), those diagnosed with CAD can reverse the progression of the disease and reduce the risk of recurrent cardiac events. Unfortunately, regardless of how successful a secondary prevention program is, they still face the prospect of living their remaining years in a diseased state. According to the vast majority of research we reviewed, there is a more attractive alternative. The best advice is to focus on primary prevention of CAD risk factors throughout youth and young adulthood, striving to reach middle age (when chronic diseases frequently begin to show) at low risk stratification.
Overall, young persons at low risk who maintain this status into middle age clearly have a lower risk of disease development and mortality rates in older ages compared with those of higher risk, despite medical interventions and treatments over the course of their lifetime (Daviglus et al. 2006). It appears that 50 may be the turning point; individuals who are able to reach this age with no risk factors have markedly higher survival rates than those with any combination of risk factors. Even individuals with one risk factor at middle age are at a much higher risk for CVD and CAD (Lloyd-Jones et al. 2007). The primary prevention of major CAD risk factors must be a first-line defense strategy in younger and middle-aged adults so that the health burden and mortality risks from CAD are lessened as one moves into older adulthood.
Sidebar: Glossary of Epidemiological Terms
all-cause mortality: annual number of deaths (all causes) in a given age group per the population in that age group.
morbidity rate: the proportion of patients with a particular disease during a given year per given unit of population.
mortality rate: an estimate of the proportion of the population that dies during a specified period, usually a year.
multifactorial: refers to the development of a condition from multiple factors.
person-years: the product of the number of years times the number of members of a population who have been affected by a certain condition.
risk factor: a characteristic statistically associated with, although not necessarily causally related to, an increased risk of morbidity or mortality.
Source: Stedman’s Online Medical Dictionary (www.stedmans.com).
Sidebar: Caloric Expenditure for the High-Risk Client: A Case Study
Frank, a 50-year-old accountant for a large corporation, is referred to you by his physician. Frank quit smoking at age 35. His family history reveals his father had two heart attacks by age 53 and his brother died of sudden cardiac death at age 49. Frank was active in college but has been inconsistent with his exercise for the last 25 years. He was diagnosed with CAD 1 year ago and had two coronary stents placed 1 month ago due to mild to moderate chest pain with activity. Frank recently completed 6 weeks of cardiac rehabilitation and has progressed well enough that he no longer needs to attend.
After Frank completed cardiac rehabilitation, a stress test measured his maximal oxygen consumption (VO2max) at 38 ml/kg/min, which is slightly above average for his age. However, Frank still needs to engage in physical activity to help prevent further problems and progression of his disease. Current lab work shows his blood pressure at 122/72 mm Hg (controlled by medication), blood sugar at 105 mg/dl, total cholesterol at 155 mg/dl (controlled by medication), LDL at 110 mg/dl, HDL at 32 mg/dl and BMI at 28 (weight is 204 pounds or 92.7 kg).
You recently came across research about ways to combat the progression of CAD. One of the articles recommended a caloric threshold range of 1,500 to stabilize existing plaque and 2,200 kcal/week to help reverse CAD. Frank’s cardiac rehabilitation program was 3 days per week, 45 minutes per session, and an additional day of walking at home for 30 minutes. You decide to increase his frequency to 5 days per week to reach an expenditure goal of 2,000 kcal/week at moderate intensity. Using the kcal/week goal, here are the steps for calculating exercise duration:
Goal: 2,000 kcal/week
Intensity: moderate (60% VO2 reserve)
Frequency: 5 days/week
Calculate target VO2 using the VO2 reserve formula:
- 38 ml/kg/min – 3.5 ml/kg/min = 34.5 ml/kg/min x (60%) = 20.7 ml/kg/min*
*For this example we are calculating net kcal expenditure, so resting VO2 (3.5 ml/kg/min) is not added back in, and our target VO2 will remain 20.7 ml/kg/min.
Calculate caloric expenditure using 20.7 ml/kg/min:
- 20.7 ml/kg/min x 92.7 kg = 1919 ml/min ├À 1,000 = 1.92 liters per minute (l/min)
- 1.92 l/min x 5 kcal/LO2 = 9.6 kcal/min
Calculate time of exercise using caloric expenditure:
- 2,000 kcal/week ├À 9.6 kcal/min = 208 min/week
- 208 min/week ├À 5 days/week = 41.6 min/day or ~42 min/day
Based on these caloric expenditure calculations, we calculated a specific exercise time for Frank per session for a moderate-intensity exercise program (60% VO2reserve). This calculated time is appropriate based on his most recent program, and it likely would not be difficult for him to complete the goal of 2,000 kcal/week. In addition, recently published public health standards (ACSM & AHA 2007) for physical activity programs recommend 5 days per week and a minimum of 30 minutes per day. This program meets those minimum standards.
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