The Effects of Aerobic Exercise and Vegan Diet on CAD: a brief review of the most current literature.
Coronary artery disease (CAD) is the most common type of heart disease and the main cause of myocardial infarctions (MI). According to the American Heart Association, 17.6 million Americans have CAD, where it affects 17% of men and 9% of women between ages 35-64 and 44% of men and 50% of women between ages 65-94.1 The disease is caused by plaque buildup along the coronary arteries, which in turn cause narrowing of the blood vessels and ischemia to the heart tissue. The major causes of CAD include hyperlipidemia (mainly elevated LDL levels), hypertension, smoking, obesity, physical inactivity, and a diet high in fat and calories, but low in phytochemicals, fiber, and vitamins C, D and E. While there is general awareness and consensus about the benefits of antiplatelet, antihypertensive and cholesterol reducing drugs as a medical treatment of CAD, there is not much emphasis about the importance of diet and exercise. Moreover, there is a lot of misinformation about which types of exercise and diets are actually effective in reducing CAD. Many recent studies have shown that diet and exercise are not only a means to prevent CAD, but are sometimes the only treatment some CAD patients need to combat this disease. The aim of this review is to evaluate these studies and elucidate which types of exercise and diet are most beneficial in decreasing and even reversing the effects of CAD.
A. Pathophysiology of CAD and link to high animal-fat diet
The pathophysiology of CAD shows how it is caused by the major risk factors discussed above, with elevated LDL being the most predominant factor. CAD is an inflammatory disease, where macrophages have been shown to play a more role in the formation of plaque and the atherosclerosis, or vessel hardening. It is believed atherosclerosis is caused by oxidation of LDL via these macrophages. Oxidized LDL can also cause an increase in platelet aggregation and has also been shown to play a role in plaque instability.2HDL, on the other hand, has been shown to have antiatherogenic effects because it reverses cholesterol transport, protects against thrombosis and maintains endothelial function.
B. The effects of a vegan diet on CAD
There are many studies that show that a low fat vegetarian diet, which helps to reduce LDL and increase HDL, not only reduces the risk of CAD, but sometimes can reverse its effects. A study conducted in 1990 showed CAD regression without the use of medications in 28 CAD patients with significant stenosis and elevated LDL that adhered to a low fat vegetarian diet.3 These patients were compared to a 20 person control. The study showed that the percentage diameter stenosis regressed from an average of 16.9% to 16.5% in the experimental group, while the control progressed from 15.5% to 18.5%. Similarly, Dod et al., who compared 27 subjects with CAD that followed a low fat vegetarian diet and lifestyle intervention, showed that the experimental group had a statistically significant reduction in C-reactive protein (common indicator of coronary artery thrombosis), and increase in endothelial-dependent flow dilatation.4
But what exactly is an ideal diet used to achieve CAD treatment? According to Dr. Dean Ornish and Dr. Caldwell Esselstyn, such a diet must be cut out of all animal fat, including diary, and be vegetable rich. This diet is different from popular “vegetarian” diets, which are grain and carbohydrate based, increasing triglyceride levels. Rather this “nutritarian” diet aims to emphasize vegetables as the main dish, along with beans and nuts as a preferable carbohydrate and healthy fat source.
The effects of Exercise on CAD
The effects of exercise on CAD have been well documented and show that 60 minutes of intense aerobic exercise at least 5 days a week reduces mortality rates in patients with previous MIs. A meta-analysis of 51 randomized control trials (RCTs) published before 1999, where a total of 8440 patients were diagnosed with CAD via angiography, and then underwent 2 months of supervised exercise, followed by 4 month of self-reported exercise regimen showed that total mortality was reduced by 27% with an exercise only intervention.5
Exercise and weight reduction have been shown to reduce LDL and increase HDL. A meta-analysis of 52 exercise training trials of greater then 12 weeks showed an average increase of HDL by 4.6% and reduction of LDL by 5% in 4700 subjects.6
Finally, exercise was also found to be beneficial to patients who were not amenable to intervention via angiography. Some studies show an improvement in symptoms, such a reduction of angina mainly due to decreased blood pressure and reduction of heart rate. Other findings indicate that exercise training alter coronary vasomotor response to exercise and thus reduce abnormal vasoconstrictive response to stress in CAD.7
1. Rosamond W, Flegal K, Furie K, et al. Heart disease and stroke statistics–2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2008; 117:e25.
2. Iuliano L, Mauriello A, Sbarigia E, et al. Radiolabeled native low-density lipoprotein injected into patients with carotid stenosis accumulates in macrophages of atherosclerotic plaque : effect of vitamin E supplementation. Circulation 2000; 101:1249.
3. Ornish, D., et al., Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial. Lancet, 1990. 336(8708): p. 129-33.
4. Dod HS, Bhardwaj R, Sajja V, et al. Effect of intensive lifestyle changes on endothelial function and on inflammatory markers of atherosclerosis. Am J Cardiol. 2010;105(3):362-367.
5. O’Conner GT, Buring JE, Yusuf S, et al. An overview of randomized trials of rehabilitation with exercise after myocardial infarction. Circulation. 1989; 80: 234-244.
6. Leon AS, Sanchez O. Meta-analysis of the effects of aerobic exercise training on blood lipids. Circulation. 2001;104(3): 2210-2216.
7. Hambrecht R, Wolf A, Gielen S, et al. Effect of exercise on coronary endothelial function in patients with CAD. N. Engl J Med. 2000;342:454-460.