Advertisement





Click here for more guidelines.
CME Topic Collections Past Issues Search Current Issue Home
     

J Am Coll Cardiol, 2005; 45:1379-1387, doi:10.1016/j.jacc.2004.11.068
© 2005 by the American College of Cardiology Foundation
This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (23)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Parikh, P.
Right arrow Articles by Sperling, L. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Parikh, P.
Right arrow Articles by Sperling, L. S.

STATE-OF-THE-ART PAPER

Diets and Cardiovascular Disease

An Evidence-Based Assessment

Parin Parikh, BA*, Michael C. McDaniel, MD{dagger}, M. Dominique Ashen, PhD, CRNP*, Joseph I. Miller, MD{dagger}, Matthew Sorrentino, MD, FACC{ddagger}, Vicki Chan, BS*, Roger S. Blumenthal, MD, FACC* and Laurence S. Sperling, MD, FACC*,*

* Department of Medicine, Johns Hopkins Ciccarone Preventive Cardiology Center, Baltimore, Maryland
{dagger} Department of Medicine, Section of Preventive Cardiology, Emory University, Atlanta, Georgia
{ddagger} University of Chicago, Department of Medicine, Section of Preventive Cardiology, Chicago, Illinois

Manuscript received September 19, 2004; revised manuscript received November 23, 2004, accepted November 29, 2004.

* Reprint requests and correspondence: Dr. Laurence Sperling, The Emory Clinic, 1525 Clifton Road, Suite 214, Atlanta, Georgia 30322 (Email: Laurence_Sperling{at}emoryhealthcare.org).


    Abstract
 Top
 Abstract
 Low-carbohydrate diets
 Glycemic index diets
 Very-low-fat (VLF) diets
 The Mediterranean Diet
 Dietary Approaches to Stop...
 Conclusions
 References
 
With rising obesity, despite low-fat diet recommendations, there is an increased interest in weight loss and alternative dietary approaches for cardiovascular health. Physicians must have an understanding of the literature to better counsel their patients about diets and cardiovascular disease. This review examines several dietary approaches to cardiovascular health and evaluates the available scientific evidence regarding these diets.

Abbreviations and Acronyms
  ALA = alpha-linolenic acid
  CVD = cardiovascular disease
  DASH = Dietary Approach to Stop Hypertension
  DHA = docosahexaenoic acid
  EPA = eicosapentaenoic acid
  GI = glycemic index
  GL = glycemic load
  HDL = high-density lipoprotein
  N3-FA = omega-3 polyunsaturated fatty acids
  VLF = very low fat


Dietary advice regarding cardiovascular disease (CVD) prevention is complex. Much confusion stems from the lack of definitive data on available diets and their potential health benefits. For years, the American Heart Association (AHA) has recommended a low-fat diet of 55% of total calories from carbohydrates, 30% from fat, and 15% from protein, with cholesterol restricted to <300 mg/day (1). However, an unintended consequence of emphasizing this low-fat diet may have been to promote unrestricted carbohydrate intake (2).

The prevalence of obesity in America increased by 61% since 1991 (3). Each year, an estimated 300,000 U.S. adults die from obesity-related causes (4), and obesity plus physical inactivity account for approximately 9.4% of U.S. health care expenditures (5). Dietary improvement may significantly impact weight and cardiovascular morbidity. Due to the increasing prevalence of obesity, despite low-fat recommendations, many new popular diets have emerged. Although some of these new diets may offer health benefits, others may potentially harm cardiovascular or overall health. Physicians must have an understanding of these diets in order to counsel patients. The goal of this paper is to review several popular dietary approaches for cardiovascular health and evaluate the available scientific evidence behind these diets.


    Low-carbohydrate diets
 Top
 Abstract
 Low-carbohydrate diets
 Glycemic index diets
 Very-low-fat (VLF) diets
 The Mediterranean Diet
 Dietary Approaches to Stop...
 Conclusions
 References
 
A low-carbohydrate diet was first characterized by William Banting in the 1860s (6), but this type of diet has currently received much attention due to Dr. Atkins’ New Diet Revolution (7). The Atkins’ Diet recommends two weeks of extreme carbohydrate restriction, followed by gradually increasing carbohydrates to 35 g/day. The Atkins’ Diet has 68% of total calories from fat, 27% from protein, and 5% from carbohydrates (8). Other popular low-carbohydrate diets are summarized in Table 1.


View this table:
[in this window]
[in a new window]
 
Table 1. Summary of Popular Low-Carbohydrate Diets*
 
Low-carbohydrate diets recommend limiting complex and simple sugars, causing the body to oxidize fat to meet energy requirements. During the initial carbohydrate restriction, the body resorts to ketosis for energy needs. Ketones are excreted in the urine with fluid. Rapid initial weight loss may be from this diuretic effect (8), which can be encouraging.

A drastic reduction in carbohydrates also leads to an overall decrease in caloric intake (9). Even when calories are not actively restricted, low-carbohydrate dieters consume fewer calories compared with baseline (10). Weight loss can be sustained by this reduction in caloric intake. Although palatable for the short term, low-carbohydrate diets raise several nutritional and cardiovascular concerns, as summarized in Table 2.


View this table:
[in this window]
[in a new window]
 
Table 2. Low-Carbohydrate Diet Pros and Cons*
 
Four randomized, controlled clinical trials (Table 3) have compared low-carbohydrate diets with low-fat diets (11–15). Although the trials differed in design, all found an average of 4 to 6 kg greater weight loss in the low-carbohydrate group at six months. However, the two studies followed to one year showed no significant weight difference (11,12).


View this table:
[in this window]
[in a new window]
 
Table 3. Low-Carbohydrate Diet and Weight Loss*
 
Foster et al. (11) conducted a randomized, controlled trial lasting one year. Sixty-three obese patients were assigned either a low-carbohydrate diet or a low-fat diet. The low-carbohydrate group showed greater weight loss at six months, but the weight loss between the groups was not significant at one year. Low-carbohydrate dieters showed a greater increase in high-density lipoprotein (HDL) cholesterol and a decrease in triglycerides that was independent of weight loss.

Stern et al. (12) conducted a one-year trial that followed 132 obese patients (body mass index ≥35 kg/m2). The subjects were randomized to a carbohydrate-restricted or fat-restricted diet. Average caloric intake decreased by 510 kcal/day in the low-carbohydrate group, but only by 97 kcal/day in the low-fat group (p = 0.183). At six months, the low-carbohydrate group showed greater weight loss, increased HDL cholesterol, decreased triglycerides, and increased insulin sensitivity. At one year, there was no difference in weight loss between the two groups, although those on the low-carbohydrate diet continued to have lower triglyceride and higher HDL cholesterol levels.

Brehm et al. (14) followed 53 female participants for six months in a randomized, controlled trial comparing a low-carbohydrate with a low-fat diet. Subjects met with a dietitian every other week and had group meetings twice a week. At six months, the low-carbohydrate group showed greater weight loss, increased HDL cholesterol, and decreased triglycerides.

Finally, Yancy et al. (15) conducted a six-month randomized, controlled trial of 120 overweight and hyperlipidemic patients. The intervention group followed a low-carbohydrate diet plus nutritional supplementation and received exercise recommendations, and the control group followed a low-fat diet. At six months, the low-carbohydrate group lost more weight than the low-fat group, and their estimated daily energy intake was 41 kcal lower. The low-carbohydrate group also had lower triglycerides and higher HDL cholesterol. However, this analysis is confounded by the nutritional supplements received by the intervention group, such as fish oils, which decrease triglyceride levels.

Bravata et al. (10) reviewed 94 low-carbohydrate diet studies. Weight loss in these studies was linked to caloric restriction, diet duration, and initial baseline weight and age. However, there was no association between weight loss and carbohydrate restriction, suggesting that short-term weight loss could instead be the result of caloric restriction and the ketosis-related diuretic effects. Of note, rapid, early weight loss, as well as the palatable nature of a low-carbohydrate diet, may act as motivating factors to remain on this type of diet (14).

Although there is no consensus on what appropriate attrition rates for clinical trials of diets should be, attrition rates of 24% to 39% (Table 4) point to the difficulty of following a low-carbohydrate diet over time. Only in one six-month trial (15) was the attrition rate in the low-carbohydrate group significantly lower (p < 0.05) than that in the low-fat group.


View this table:
[in this window]
[in a new window]
 
Table 4. Attrition Rates in Randomized, Controlled Trials*
 
Low-carbohydrate diets may increase HDL cholesterol, decrease triglyceride levels, and improve glycemic control, but there appears to be no significant difference in weight loss compared with a low-fat diet at one year. Because the longest trial extends to one year with relatively few subjects, more studies are required to assess the efficacy of a low-carbohydrate diet on long-term weight loss and cardiovascular outcomes.


    Glycemic index diets
 Top
 Abstract
 Low-carbohydrate diets
 Glycemic index diets
 Very-low-fat (VLF) diets
 The Mediterranean Diet
 Dietary Approaches to Stop...
 Conclusions
 References
 
The glycemic index (GI) is a concept that has been used in diets such as the South Beach Diet (16), Sugar Busters (17), and the Zone Diet (18). These diets allow carbohydrate consumption as long as they have a low GI. The GI is a measure of the blood glucose response to intake of a particular carbohydrate (19). The higher the peak in postprandial blood glucose levels, the higher the GI value. The glycemic load (GL) is the product of dietary GI and total dietary carbohydrate, providing a useful measure of the total glycemic effect (20). Table 5 shows a list of common foods and their associated GI and GL. A high-GI diet has been proposed to increase hunger and elevate free fatty acid levels, leading to an increased risk of obesity, diabetes, and CVD (21). Several in vitro experiments indicate that elevated postprandial blood glucose levels cause oxidative stress, leading to endothelial damage and activation of coagulation (22).


View this table:
[in this window]
[in a new window]
 
Table 5. Glycemic Index and Glycemic Loads of Various Foods*
 
The framework of the South Beach Diet includes an initial two-week period of extreme carbohydrate restriction followed by gradual re-introduction of low-GI carbohydrates. The maintenance phase encourages intake of fruits, vegetables, whole grains, mono- and polyunsaturated fats, omega-3 fatty acids, nuts, and moderate dairy products. Unlike the Atkins’ Diet, the South Beach Diet encourages lean protein, such as fish and poultry, and allows olive oil as a source of mono- and polyunsaturated fat.

The longest interventional study conducted in humans related to GI was a crossover study lasting 12 weeks (23). Thirty women were randomized to a low-GI or high-GI diet. Those on a high-GI diet lost 7.4 kg, whereas those on a low-GI diet lost 9.4 kg (p = 0.14). In 16 women who participated in a 12-week follow-up, crossover study, those on a low-GI diet lost 7.4 kg, compared with 4.5 kg on a high-GI diet (p < 0.05). However, the results from other interventional studies, although shorter in duration and with smaller populations, have been inconsistent (24).

A possible association between a high-GI diet and diabetes has been observed. Studies that investigated this relationship include the Nurses’ Health Study (25), which followed over 65,000 U.S. women for six years, the Health Professionals’ Survey (26), which followed 42,750 U.S. men for six years, and the Iowa Women’s Health Study, which followed 36,000 women for six years (27). All of these prospective cohort studies showed an association between diabetes and high GL. A recent meta-analysis of 14 randomized, controlled trials comparing low- and high-GI diets in diabetes management showed that glycated proteins were reduced 7.4% on a low-GI diet (28). Multiple cohort studies (Table 6) have been inconclusive as to whether a high-GI diet may also be linked to CVD risk factors (29–33).


View this table:
[in this window]
[in a new window]
 
Table 6. Cohort Studies Investigating Low-Glycemic Index and Cardiovascular Disease Risk*
 
High-GI diets may alter HDL metabolism. A survey of 1,420 British adults (32) evaluated GI through a seven-day diet survey and showed an inverse relationship between GI and HDL cholesterol. The Third National Health and Nutrition Examination Survey (NHANES III) (33), which followed 13,907 subjects older than 20 years old, demonstrated that for every 15-U increase in GI, there was a 0.06-mmol/l decrease in HDL cholesterol.

Many of these prospective cohort studies contain confounding variables. Most of these studies based their GI and GL calculations on self-reporting. Portion size and recall bias could result in inaccurate reporting (24). Also, the GI of a food can change depending on the method of food preparation and different types of the same food (i.e., different grains of rice). Despite suggestive evidence, no trials have shown that low-GI diets prevent CVD. Longer studies with more participants are needed before low-GI diets can be definitively recommended.


    Very-low-fat (VLF) diets
 Top
 Abstract
 Low-carbohydrate diets
 Glycemic index diets
 Very-low-fat (VLF) diets
 The Mediterranean Diet
 Dietary Approaches to Stop...
 Conclusions
 References
 
Very-low-fat (VLF) diets allow less than 15% of total calories from fat (with an equal distribution of saturated, monounsaturated, and polyunsaturated fats), 15% from protein, and 70% from carbohydrates. The VLF diet includes variations of vegetarian diets that may include eggs and dairy. Although an AHA scientific statement concluded there were little long-term data to suggest that low-fat diets alone will sustain long-term weight loss, there is evidence that this diet can impact cardiovascular risk (34).

The Heidelberg trial (35) evaluated 113 patients with stable angina. The experimental group reduced fat to <20% of calories and total cholesterol to <200 mg/dl and engaged in moderate-intensity exercise. After 12 months, the intervention group’s body weight decreased by 5% (p < 0.001), total cholesterol by 10% (p < 0.001), and triglycerides by 24% (p < 0.001). In the intervention group, progression of coronary lesions by angiography was decreased compared with that of controls (p < 0.05). However, given the confounding effects of exercise, this study makes it difficult to assess the effects of diet alone.

The Pritikin diet recommends <10% of calories from fat, 15% to 20% from protein, and the remainder from unrefined, complex carbohydrates. In a small three-week study combining statins, diet, and vigorous exercise, those on the Pritikin diet resulted in a further 19% reduction in total cholesterol. There was also an incremental benefit in low-density lipoprotein (LDL) cholesterol and triglycerides for those on the diet, but also a slight reduction in HDL cholesterol (36).

The Ornish Lifestyle Heart Trial (37) randomized 48 patients with moderate to severe coronary heart disease (CHD) to intensive life-style changes or usual care. The intensive life-style changes included a vegetarian diet with 7% of caloric intake coming from fat, moderate aerobic exercise, stress management training, smoking cessation, and group psychosocial support. A total of 195 coronary artery lesions were analyzed angiographically. Overall, 82% of experimental group patients had an average change toward lesion regression. At five years, there were 2.5 times fewer cardiac events in the intervention group, and the average percent diameter stenosis showed an 8% decrease in diameter, whereas the control group had 28% progression. However, the data are difficult to interpret due to the confounding effects of exercise, stress reduction, and 11-kg weight loss in the intervention group. Although the intervention seems beneficial, the small sample size and intense life-style changes raise concerns about the universal sustainability of such a program.

The VLF diet and intense life-style changes have significant results in terms of reducing risk factors and cardiac event rates. However, these studies are relatively small, and the programs involved may be influenced by selection bias. The programs require a motivated group of patients to undergo rigorous life-style adjustments. The VLF diet may be unnecessary if other life-style characteristics like exercise, smoking cessation, and stress management are optimized.


    The Mediterranean Diet
 Top
 Abstract
 Low-carbohydrate diets
 Glycemic index diets
 Very-low-fat (VLF) diets
 The Mediterranean Diet
 Dietary Approaches to Stop...
 Conclusions
 References
 
The Mediterranean Diet is characterized by (38): 1) an abundance of plant food (fruit, vegetables, breads, cereals, potatoes, beans, nuts, and seeds); 2) minimally processed, seasonally fresh, locally grown foods; 3) desserts comprised typically of fresh fruit daily and occasional sweets containing refined sugars or honey; 4) olive oil (high in polyunsaturated fat) as the principal source of fat; 5) daily dairy products (mainly cheese and yogurt) in low to moderate amounts; 6) fish and poultry in low to moderate amounts; 7) up to four eggs weekly; 8) red meat rarely; and 9) and wine in low to moderate amounts with meals.

Although a Mediterranean-style diet has demonstrated greater weight reduction compared with control diets in randomized, controlled trials (39), the most impressive benefits of the diet are related to cardiovascular morbidity and mortality. No isolated aspect of the Mediterranean Diet explains these benefits, but much has focused on the omega-3 polyunsaturated fatty acids (N-3 FA). Examples of N-3 FA include eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) found in fatty fish like salmon, mackerel, herring, and trout (40). A form of N-3 FA derived from plants—alpha-linolenic acid (ALA)—is found in nuts, canola (rapeseed) oil, flaxseed, flaxseed oil, and soybean oil (40). Alpha-linolenic acid can be converted to EPA and DHA (41), which are thought be cardioprotective (41–46).

One major mechanism of protection may be related to the anti-arrhythmic effects of N-3 FA (47). Data from various animal, epidemiologic, and metabolic studies, as well as smaller clinical trials, demonstrate the benefits of N-3 FA in reducing the risk of sudden cardiac death (48). Omega-3 polyunsaturated fatty acids also decrease the arachidonic acid content of cell membranes, reduce eicosanoids, downregulate gene expression of adhesion molecules, and inhibit the synthesis of proinflammatory cytokines such as tumor necrosis factor-alpha, interleukin (IL)-1, and IL-2 (49). Moreover, fish oil supplements can lower triglycerides, inhibit endothelial cell activation, and improve endothelial function in diabetics (50). They can also reduce platelet aggregation (51) and decrease the heart rate (52).

Multiple randomized, controlled trials have demonstrated the benefits of the Mediterranean Diet on secondary prevention of CVD (Table 7) (53–57). The Diet and Reinfarction Trial (DART) (49) followed 2,000 men for two years to study the effect on the secondary prevention of myocardial infarction (MI). The men were randomized to four groups. One group received advice in accordance with AHA dietary guidelines. Another group was advised to consume fish twice per week (300 g total) in order to achieve approximately 2.5 g of EPA weekly. A third group was told to increase cereal fiber intake to 18 g/day. A fourth group (controls) did not receive advice. In comparing the four groups, the fish group showed a 29% reduction in mortality compared with the control group. The rate of fatal MI was also less in the fish group.


View this table:
[in this window]
[in a new window]
 
Table 7. Summary of Randomized, Controlled Trials With Mediterranean-Style Diets*
 
The Lyon Diet Heart Study (56) randomized 605 participants with a previous MI for 46 months and showed an inverse relationship between ALA intake and the risk of a second MI. The intervention group was advised to eat more fish, fruits, and vegetables and to use an ALA-rich margarine. The control group was advised to follow a prudent diet. There was a 68% decrease in primary end points (cardiac death and nonfatal MI). Secondary end points (periprocedural infarctions, unstable angina, heart failure, stroke, and pulmonary or peripheral embolisms) also decreased. Of note, at four-year follow-up, most experimental patients were still closely following the recommended diet.

The largest randomized, controlled trial examining the benefits of fish oil supplements was the GISSI-Prevenzione trial (57), which followed 11,234 subjects for a mean of 42 months. Participants were randomized to four groups, with subjects receiving a placebo, fish oil supplements equivalent to 1 g of EPA/DHA per day, 300 mg of vitamin E per day, or both the fish oil supplements and vitamin E. The investigators found no effect of vitamin E on CVD. In the experimental group, there was an approximate 20% reduction over 3.5 years in cardiac death, nonfatal MI, and nonfatal stroke. The greatest benefit was seen in sudden cardiac death, with reductions of 35% to 45%.

Multiple prospective cohort studies (Table 8) support the benefit of a Mediterranean-style diet (58–60). Most recently, 22,043 patients from a Greek population completed a questionnaire for the European Prospective Investigation into Cancer and Nutrition (61). Investigators used a scale of 0 to 9 to estimate adherence to the Mediterranean Diet, with higher scores reflecting greater adherence. After a mean follow-up of 44 months, each two-point increment in adherence to the diet was associated with a 25% reduction in total mortality. Greater compliance was associated with reductions in CHD and cancer mortality. This study points to the possible synergistic effect of the Mediterranean Diet as a whole, rather than protective effects of any one aspect.


View this table:
[in this window]
[in a new window]
 
Table 8. Large Prospective Cohort Studies Investigating the Mediterranean Diet*
 
There is consistent basic science and clinical trial evidence for the cardioprotective effects of the Mediterranean Diet, particularly in secondary prevention of acute and fatal MI. Patients on a Mediterranean diet have been shown to lose more weight, have lower C-reactive protein levels, have less insulin resistance, have lower total cholesterol and triglyceride and higher HDL levels, and have a decreased prevalence of the metabolic syndrome (39). Although attrition data are not available for all the trials, the Lyon Diet Heart trial concluded most experimental patients were still closely following the recommended diet at four years (56). The AHA guidelines recommend consuming 1 g/day of EPA/DHA; however, it is quite difficult to sustain this level with fish consumption alone (40). Based on the GISSI trial, the AHA and others (62) have therefore recommended taking supplements of three 1-g fish oil capsules per day.

In regard to primary prevention, studies show that a Mediterranean diet may be linked to decreased rates of sudden cardiac death, CHD, and possibly overall mortality. A systematic review by Hu and Willet (52) of metabolic, epidemiologic, and clinical trial evidence indicated that three dietary strategies are effective in preventing CHD: 1) substituting non-hydrogenated unsaturated fats for saturated and trans-fats; 2) increasing consumption of omega-3 fatty acids; and 3) consuming more fruits, vegetables, nuts, and whole grains, while avoiding refined grain products.

There are some concerns regarding the Mediterranean Diet. Potential side effects of the diet include a fishy aftertaste, gastrointestinal discomfort, and possibly an increase in LDL cholesterol (40). Another concern is mercury exposure. In fact, the Food and Drug Administration (FDA) currently recommends that children and women who are pregnant and/or lactating should avoid fish consumption (40).


    Dietary Approaches to Stop Hypertension (DASH)
 Top
 Abstract
 Low-carbohydrate diets
 Glycemic index diets
 Very-low-fat (VLF) diets
 The Mediterranean Diet
 Dietary Approaches to Stop...
 Conclusions
 References
 
The DASH Diet is similar to a Mediterranean-type diet, emphasizing high intake of fruits, vegetables, low-fat dairy products, whole grains, nuts, fish, and poultry, as well as reducing total and saturated fats. Reduced intake of red meat, sweets, and sugar-containing beverages is encouraged, which results in a diet high in potassium, calcium, magnesium, and fiber. This dietary approach has been shown to lower blood pressure, but little has been published regarding weight loss.

The original DASH trial (63) consisted of 459 subjects with systolic blood pressures <160 mm Hg and diastolic blood pressures between 80 and 95 mm Hg. For three weeks, all participants were fed a control diet low in fruits, vegetables, and dairy products, and with a fat content typical of an American diet (37% of daily caloric intake). During the following eight weeks, the participants were randomized to one of three diets: the control diet, a diet rich in fruits and vegetables, or the DASH Diet.

The DASH Diet reduced systolic blood pressure by 5.5 mm Hg and diastolic blood pressure by 3.3 mm Hg, as compared with controls. Subgroup analysis showed that African Americans and those with hypertension had the greatest reduction in blood pressure. The DASH diet results might be applied to a larger group due to the heterogeneous population: half of the participants were women, 60% were African American, and 37% had household incomes of <$30,000 per year. One limitation of applying the DASH Diet to the general population is that the study was carried out in a very controlled setting, where all the meals were prepared for the subjects, and thus no comments may be made regarding attrition rates for the diet.

The DASH Diet was not low in sodium, but still reduced blood pressure. A meta-analysis of 56 randomized, controlled trials that included over 3,500 participants did not support universal sodium restriction, but instead only recommended dietary sodium restriction in the elderly (64).

To further investigate the effects of sodium restriction, the DASH-Sodium Trial (65) was conducted. A total of 412 subjects were randomized to the control diet or DASH diet for 90 days. Within each arm, patients were further stratified and assigned to three diets: high (3.5 g/day), intermediate (2.3 g/day), or low (1.2 g/day) sodium, each for a 30-day period in a random order. In the control group, there was a dose response with the greater reductions in sodium intake correlating with greater decreases in blood pressure. For those on the DASH Diet, the dose response persisted, although the effects of sodium reduction were smaller. Additionally, there was no significant difference between high and intermediate sodium intake on diastolic blood pressure for those on the DASH Diet. The difference was only significant between the high- and low-sodium groups. The DASH Diet can reduce systolic blood pressure by 5.5 mm Hg and diastolic blood pressure by 3.3 mm Hg. However, the effect of sodium reduction on hypertension remains controversial. Lowering sodium to the levels of 1.2 g/day, as achieved in the lowest sodium intake group of the DASH-Sodium Trial, would be nearly impossible without changes in the food industry, as 75% of sodium intake comes from additions made in processing (66).


    Conclusions
 Top
 Abstract
 Low-carbohydrate diets
 Glycemic index diets
 Very-low-fat (VLF) diets
 The Mediterranean Diet
 Dietary Approaches to Stop...
 Conclusions
 References
 
Physicians and patients are continually searching for optimal methods to lose weight and maintain a diet that sustains cardiovascular health. Patient frustration with current AHA and National Cholesterol Education Program (NCEP) low-fat guidelines has been evident by poor compliance to these recommended diets and the increasing prevalence of obesity. The scientific community has also begun to question the low-fat diet-heart hypothesis (67). A few summary points (Table 9) can be extracted from this review.


View this table:
[in this window]
[in a new window]
 
Table 9. Diet Summary Points
 
A low-carbohydrate diet can lead to short-term weight loss. However, the long-term effects on CHD risk factors, such as weight loss, HDL and LDL cholesterol, triglycerides, glycemic control, and blood pressure, are unknown.

Moderate-sized studies on VLF diets show decreases in cardiovascular events, but the sustainability and applicability of these diets to a large population is a concern. Moreover, as many of these studies also included life-style changes as part of the treatment, it is not possible to separate these effects from those of the diet itself.

No adequate randomized, controlled trials have evaluated the effects of a low-GI diet on CVD. Nonetheless, diets based on a low GI, such as the South Beach Diet, can encourage consumption of mono- and polyunsaturated fats, lean protein, fruits, vegetables, and whole-grain foods instead of simple, refined carbohydrates.

The Mediterranean Diet has been shown to be cardioprotective in both prevention of sudden cardiac death and secondary prevention.

The DASH Diet, which has shown to reduce blood pressure, fits well into the framework of a Mediterranean Diet and can help decrease the cardiovascular risk of hypertension.

Although none of the reviewed diets are independently perfect for weight loss and cardiovascular health, an optimal diet can be extracted from this review. Specifically, such a diet would encourage: 1) decreased carbohydrate intake, especially of refined and high-GI carbohydrates; 2) increased consumption of fruits, vegetables, and whole grains; 3) increased intake of polyunsaturated fats by increasing consumption of plant oils and fish; 4) and moderate intake of low-fat dairy products and nuts.

Although many patients desire quick weight loss, patients should understand the basic concept that food is fuel, and people will lose weight if they burn more calories than they consume. Just as patients should not restrict fat and eat unrestricted amounts of carbohydrates, patients should not decrease carbohydrates and eat unrestricted amounts of fat. Portion size and total caloric intake is often more important than individual foods.

In place of the traditional USDA food pyramid, the Mayo Clinic has published an alternative healthy weight food pyramid (Fig. 1) (68). This pyramid illustrates an updated version of a properly balanced diet and promotes a healthy and sustainable dietary change instead of relying on short-term diets (69), recommendations supported by the evidence presented in this review. By encouraging patients to adopt an active lifestyle and to lose weight gradually using an evidence-based dietary approach, physicians can better counsel patients toward improved cardiovascular health.



View larger version (73K):
[in this window]
[in a new window]
 
Figure 1 The Mayo Clinic Healthy Weight Pyramid is a tool to help lose weight or maintain weight. The pyramid offers a somewhat different approach to healthy eating compared with the USDA Food Guide Pyramid. It focuses on low energy-dense foods, which have a small number of calories in a large amount of food. The foundation of the pyramid is unlimited amounts of vegetables and fruits (minimum four servings per day). One serving of vegetables equals 25 calories; one serving of fruit equals 60 calories. Level two in the pyramid is carbohydrates, including whole grains (four to eight servings per day). One serving of carbohydrate equals 70 calories. Protein/dairy is the third level of the pyramid (three to seven servings per day). One serving equals 70 calories. Fats, the fourth level of the pyramid, include heart-healthy olive oil, nuts, canola oil, and avocados (three to five servings per day). One serving of fat equals 45 calories.

 


    References
 Top
 Abstract
 Low-carbohydrate diets
 Glycemic index diets
 Very-low-fat (VLF) diets
 The Mediterranean Diet
 Dietary Approaches to Stop...
 Conclusions
 References
 
1. Krauss RM, Eckel RH, Howard B, et al. AHA dietary guidelines, revision 2000a statement for healthcare professionals from the Nutrition Committee of the American Heart Association. Circulation 2000;102:2296-2311.

2. Weinber SL. The diet-heart hypothesisa critique. J Am Coll Cardiol 2004;43:731-733.[Abstract/Free Full Text]

3. Mokdad AH, Bowman BA, Ford ES, et al. The continuing epidemics of obesity and diabetes in the United States JAMA 2001;286:1195-1200.[Abstract/Free Full Text]

4. Allison D, Fontaine K, Manson J, Stevens J, VanItallie T. Annual deaths attributable to obesity in the United States JAMA 1999;282:1530-1538.[Abstract/Free Full Text]

5. Colditz G. Economic costs of obesity and inactivity Med Sci Sports Exerc 1999;31(Suppl 11)S663–7.

6. Banting W. Letter on Corpulence, Addressed to the Public2nd edition. London: Harisson and Sons; 1863.

7. Atkins RC. Dr. Atkins’ New Diet RevolutionNew York, NY: Avon Books; 1998.

8. St. Jeor ST, Howard BV, Prewitt TE, et al. Dietary protein and weight reductiona statement for healthcare professionals from the Nutrition Committee of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation 2001;104:1869-1874.[Abstract/Free Full Text]

9. Bonow RO, Eckel RH. Diet, obesity, and cardiovascular risk N Engl J Med 2003;348:2057-2058.[Free Full Text]

10. Bravata DM, Sander L, Huang J, et al. Efficacy and safety of low-carbohydrate dietsa systematic review. JAMA 2003;289:1837-1850.[Abstract/Free Full Text]

11. Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity N Engl J Med 2003;348:2082-2090.[Abstract/Free Full Text]

12. Stern L, Iqbal N, Seshadri P, et al. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adultsone-year follow-up of a randomized trial. Ann Intern Med 2004;140:778-785.[Abstract/Free Full Text]

13. Samaha FF, Iqbal N, Seshadri P, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity N Engl J Med 2003;348:2074-2081.[Abstract/Free Full Text]

14. Brehm BJ, Seeley RJ, Daniels SR, D’Alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women J Clin Endocrinol Metab 2003;88:1617-1623.[Abstract/Free Full Text]

15. Yancy WS, Olsen MK, Guyton JR, et al. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia Ann Intern Med 2004;140:769-777.[Abstract/Free Full Text]

16. Agatston A. The South Beach DietThe Delicious, Doctor-Designed, Foolproof Plan for Fast and Healthy Weight Loss. New York, NY: Rodale; 2003.

17. Sugar Busters! Concept 2004http://www.sugarbusters.com/filessb/concept.html. Accessed May 11.

18. ZonePerfect Nutrition Program 2004http://www.zoneperfect.com/site/content/guide_02_ZoneDiet.asp. Accessed May 11.

19. Jenkins DJA, Thomas DM, Wolever S, et al. Glycemic index of fooda physiological basis for carbohydrate exchange. Am J Clin Nutr 1981;34:362-366.[Abstract/Free Full Text]

20. Jenkins DJA, Kendall CWC, Augustin LSA, et al. Glycemic indexoverview of implications in health and disease. Am J Clin Nutr 2002;76:266S-273S.[Abstract/Free Full Text]

21. Foster-Powell K, Holt SHA, Brand-Miller JC. International table of glycemic index and glycemic load values2002. Am J Clin Nutr 2002;76:5-56.[Abstract/Free Full Text]

22. Lefebvre PJ, Scheen AJ. The postprandial state and risk of cardiovascular disease Diabet Med 1998;15:S63-S68.

23. Slabber M, Barnard HC, Kuyl JM, Dannhauser A, Schall R. Effects of a low-insulin-response, energy-restricted diet on weight loss and plasma insulin concentrations in hyperinsulinemic obese females Am J Clin Nutr 1994;60:48-53.[Abstract/Free Full Text]

24. Pi-Sunyer FX. Glycemic index and disease Am J Clin Nutr 2002;76:290S-298S.[Abstract/Free Full Text]

25. Salmeron J, Manson JE, Stampfer MJ, et al. Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women JAMA 1997;277:472-477.[Abstract/Free Full Text]

26. Salmeron J, Ascherio A, Rimm EB, et al. Dietary fiber, glycemic load, an risk of NIDDM in men Diabetes Care 1997;20:545-550.[Abstract]

27. Meyer KA, Kushi LH, Jacobs DR, Slavin J, Sellers TA, Folsom AR. Carbohydrates, dietary fiber, and incident type 2 diabetes in older women Am J Clin Nutr 2000;71:921-930.[Abstract/Free Full Text]

28. Brand-Miller J, Hayne S, Petocz P, Colagiuri S. Low-glycemic index diets in the management of diabetesa meta-analysis of randomized controlled trials. Diabetes Care 2003;26:2261-2267.[Abstract/Free Full Text]

29. Liu S, Willett WC, Stampfer MJ, et al. A prospective study of dietary glycemic load, carbohydrate intake, and risk of coronary heart disease in U.S. women Am J Clin Nutr 2000;71:1455-1461.[Abstract/Free Full Text]

30. van Dam RM, Visscher AW, Feskens EJ, Verhoef P, Kromhout D. Dietary glycemic index in relation to metabolic risk factors and incidence of coronary heart diseasethe Zutphen Elderly Study. Eur J Clin Nutr 2000;54:726-731.[CrossRef][Web of Science][Medline]

31. Tavani A, Bosetti C, Negri E, Augustin LS, Jenkins DJA, La Vecchia C. Carbohydrates, dietary glycaemic load and glycaemic index, and risk of acute myocardial infarction Heart 2003;89:722-726.[Abstract/Free Full Text]

32. Frost G, Leeds AA, Doré CJ, Madeiros S, Brading S, Dornhorst A. Glycaemic index as a determinant of serum HDL-cholesterol concentration Lancet 1999;353:1045-1048.[CrossRef][Web of Science][Medline]

33. Ford ES, Liu S. Glycemic index and serum high-density lipoprotein cholesterol concentration among U.S. adults Arch Intern Med 2001;161:572-576.[Abstract/Free Full Text]

34. Lichtenstein AH, Van Horn L. AHA science advisoryvery low fat diets. Circulation 1998;98:935-939.[Free Full Text]

35. Niebauer J, Hambrecht R, Marburger C, et al. Impact of intensive physical exercise and low-fat diet on collateral vessel formation in stable angina pectoris and angiographically confirmed coronary artery disease Am J Cardiol 1995;76:771-775.[CrossRef][Web of Science][Medline]

36. Barnard RJ, DiLauro SC, Inkeles SB. Effects of intensive diet and exercise intervention in patients taking cholesterol-lowering drugs Am J Cardiol 1997;79:1112-1114.[CrossRef][Web of Science][Medline]

37. Ornish D, Scherwitz LW, Billings JH. Intensive lifestyle changes for reversal of coronary heart disease JAMA 1998;280:2001-2007.[Abstract/Free Full Text]

38. Hu FB. The Mediterranean Diet and mortality—olive oil and beyond N Engl J Med 2003;348:2595-2596.[Free Full Text]

39. Esposito K, Marfella R, Ciotola M, et al. Effect of a Mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome JAMA 2004;292:1440-1446.[Abstract/Free Full Text]

40. Kris-Etherton PM, Harris WS, Appel LJ, et al. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease Circulation 2002;106:2747-2757.[Free Full Text]

41. Grundy SM. N-3 fatty acidspriority for post-myocardial infarction clinical trials. Circulation 2003;107:1834-1836.[Free Full Text]

42. Das UN. Beneficial effect(s) of n-3 fatty acids in cardiovascular diseasebut why and how?. Prostaglandins Leukot Essent Fatty Acids 2001;63:351-362.

43. Calder PC, Grimble RF. Polyunsaturated fatty acids, inflammation and immunity Eur J Clin Nutr 2002;56(Suppl 3):S14-S19.

44. Leaf A. The electrophysiologic basis for the anti-arrhythmic and anticonvulsant effects of n-3 polyunsaturated fatty acidsheart and brain. Lipids 2001;36(Suppl):S107-S110.

45. Schoene NW. Vitamin E and omega-3 fatty acidseffectors of platelet responsiveness. Nutrition 2001;17:793-796.[CrossRef][Web of Science][Medline]

46. Mori TA, Beilin LJ. Long-chain omega-3 fatty acids, blood lipids and cardiovascular risk reductions Curr Opin Lipidol 2001;12:11-17.[CrossRef][Web of Science][Medline]

47. Leaf A, Kang JX, Xiao Y, Billman GE. Clinical prevention of sudden cardiac death by n-3 polyunsaturated fatty acids and mechanism of prevention of arrhythmias by n-3 fish oils Circulation 2003;107:2626-2652.

48. Kang JX, Leaf A. Prevention of fatal cardiac arrhythmias by polyunsaturated fatty acids Am J Clin Nutr 2000;71:202S-207S.[Abstract/Free Full Text]

49. von Shacky C. N-3 fatty acids and prevention of coronary atherosclerosis Am J Clin Nutr 2000;71:224S-227S.[Abstract/Free Full Text]

50. Brown A, Hu FB. Dietary modulation of endothelial function Am J Clin Nutr 2001;73:673-686.[Abstract/Free Full Text]

51. Dallongeville J, Yarnell J, Ducimetiere P, et al. Fish consumption is associated with lower heart rates Circulation 2003;108:820-825.[Abstract/Free Full Text]

52. Hu FB, Willett WC. Optimal diets for prevention of coronary heart disease JAMA 2002;288:2569-2578.[Abstract/Free Full Text]

53. Singh RB, Niaz MA, Sharma JP, Kumar R, Rastogi V, Moshiri M. Randomized, double-blind, placebo-controlled trial of fish oil and mustard oil in patients with suspected acute myocardial infarctionthe Indian Experiment of Infarct Survival-4. Cardiovas Drugs Ther 1997;11:485-491.[CrossRef][Web of Science][Medline]

54. Singh RB, Dubnov G, Niaz MA, et al. Effect of an Indo-Mediterranean diet on progression of coronary artery disease in high risk patients (Indo-Mediterranean Diet Heart Study)a randomized single-blind trial. Lancet 2002;360:1455-1461.[CrossRef][Web of Science][Medline]

55. Burr ML, Gilbert JH, Holliday RM, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarctionDiet and Reinfarction Trial (DART). Lancet 1989;2:757-761.[Web of Science][Medline]

56. de Lorgeril M, Salen P, Martin JL, Monjaud I, Delaye J, Mamelle N. Mediterranean Diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarctionfinal report of the Lyon Diet Heart Study. Circulation 1999;99:779-785.[Abstract/Free Full Text]

57. The GISSI-Prevenzione Investigators Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarctionresults of the GISSI-Prevenzione trial. Lancet 1999;354:447-455.[CrossRef][Web of Science][Medline]

58. Hu FB, Bronner L, Willett WC, et al. Fish and omega-3 fatty acid intake and risk of coronary heart disease in women JAMA 2002;287:1815-1821.[Abstract/Free Full Text]

59. Albert CM, Campos H, Stampfer MJ, et al. Blood levels of long-chain n-3 fatty acids and the risk of sudden death N Engl J Med 2002;346:1113-1118.[Abstract/Free Full Text]

60. Lemaitre RN, King IB, Mozaffarian D, et al. n-3 Polyunsaturated fatty acids, fatal ischemic heart disease, and nonfatal myocardial infarction in older adultsthe Cardiovascular Health Study. Am J Clin Nutr 2003;77:319-325.[Abstract/Free Full Text]

61. Trichopoulou A, Costacou T, Bamia C, Trichopoulos D. Adherence to a Mediterranean Diet and survival in a Greek population N Engl J Med 2003;348:2599-2608.[Abstract/Free Full Text]

62. Harris WS. N-3 long-chain polyunsaturated fatty acids reduce risk of coronary heart disease deathextending evidence to the elderly. Am J Clin Nutr 2003;77:279-280.[Free Full Text]

63. Appel LJ, Moore TJ, Obarzenek E, et al. A clinical trial of the effects of dietary patterns on blood pressure N Engl J Med 1997;336:1117-1124.[Abstract/Free Full Text]

64. Midgley JP, Matthew AG, Greenwood CM, Logan AG. Effect of reduced dietary sodium on blood pressurea meta-analysis of randomized controlled trials. JAMA 1996;275:1590-1597.[Abstract/Free Full Text]

65. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) Diet N Engl J Med 2001;344:3-10.[Abstract/Free Full Text]

66. Whelton PK, He J, Appel LJ, et al. Primary prevention of hypertensionclinical and public health advisory from the National High Blood Pressure Program. JAMA 2002;288:1882-1888.[Abstract/Free Full Text]

67. Weinberg SL. The Diet-Heart Hypothesisa critique. J Am Coll Cardiol 2004;43:731-733.[Abstract/Free Full Text]

68. Mayo Clinic Healthy Weight Pyramid 2004http://www.mayoclinic.org/news2000-av/pyramid.jpg. Accessed May 11.

69. Willett WC. Reduced-carbohydrate dietsno roll in weight management?. Ann Intern Med 2004;140:836-837.[Free Full Text]




This article has been cited by other articles:


Home page
Am. J. Clin. Nutr.Home page
F. Imamura, P. F Jacques, D. M Herrington, G. E Dallal, and A. H Lichtenstein
Adherence to 2005 Dietary Guidelines for Americans is associated with a reduced progression of coronary artery atherosclerosis in women with established coronary artery disease
Am. J. Clinical Nutrition, July 1, 2009; 90(1): 193 - 201.
[Abstract] [Full Text] [PDF]


Home page
Diabetes and Vascular Disease ResearchHome page
J.-C. Fruchart, F. M Sacks, M. P Hermans, G. Assmann, W V. Brown, R. Ceska, M J. Chapman, P. M Dodson, P. Fioretto, H. N Ginsberg, et al.
The Residual Risk Reduction Initiative: a call to action to reduce residual vascular risk in dyslipidaemic patients
Diabetes and Vascular Disease Research, November 1, 2008; 5(4): 319 - 335.
[Abstract] [PDF]


Home page
Scand J Public HealthHome page
T. Mildestvedt, E. Meland, and G. E. Eide
No difference in lifestyle changes by adding individual counselling to group-based rehabilitation RCT among coronary heart disease patients
Scand J Public Health, December 1, 2007; 35(6): 591 - 598.
[Abstract] [PDF]


Home page
Cardiovasc ResHome page
C. Napoli, W. C. Stanley, and L. J. Ignarro
Nutrition and cardiovascular disease: Putting a pathogenic framework into focus
Cardiovasc Res, January 15, 2007; 73(2): 253 - 256.
[Full Text] [PDF]


Home page
Am J Crit CareHome page
A. G. Rosenfeld
State of the Heart: Building Science to Improve Women's Cardiovascular Health
Am. J. Crit. Care., November 1, 2006; 15(6): 556 - 566.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
I. G.E. Zarraga and E. R. Schwarz
Impact of Dietary Patterns and Interventions on Cardiovascular Health
Circulation, August 29, 2006; 114(9): 961 - 973.
[Full Text] [PDF]


Home page
J Am Coll CardiolHome page
D. Giugliano, A. Ceriello, and K. Esposito
The Effects of Diet on Inflammation: Emphasis on the Metabolic Syndrome
J. Am. Coll. Cardiol., August 15, 2006; 48(4): 677 - 685.
[Abstract] [Full Text] [PDF]


Home page
Arch Intern MedHome page
A. J. Nordmann, A. Nordmann, M. Briel, U. Keller, W. S. Yancy Jr, B. J. Brehm, and H. C. Bucher
Effects of Low-Carbohydrate vs Low-Fat Diets on Weight Loss and Cardiovascular Risk Factors: A Meta-analysis of Randomized Controlled Trials.
Arch Intern Med, February 13, 2006; 166(3): 285 - 293.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
H. Schroeter, C. Heiss, J. Balzer, P. Kleinbongard, C. L. Keen, N. K. Hollenberg, H. Sies, C. Kwik-Uribe, H. H. Schmitz, and M. Kelm
(-)-Epicatechin mediates beneficial effects of flavanol-rich cocoa on vascular function in humans
PNAS, January 24, 2006; 103(4): 1024 - 1029.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (23)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Parikh, P.
Right arrow Articles by Sperling, L. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Parikh, P.
Right arrow Articles by Sperling, L. S.

 
  CME Topic Collections Past Issues Search Current Issue Home

Advertisement