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Dietary Sodium Intake and Subsequent Risk of Cardiovascular Disease in Overweight Adults (Richard Adefioye)

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Dietary Sodium Intake and Subsequent Risk of Cardiovascular Disease in Overweight Adults (Richard Adefioye)

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This study sought to examine the risk of cardiovascular disease associated with dietary sodium intake in overweight and non-overweight persons.

I feel this article is important because sodium (salt) is a pretty common component of the standard American diet, which many people consume.

This study contained 14, 407 participants aged 25-74 years. The results showed that among overweight persons with an average energy intake of 7452 kJ, a 100 mmol higher sodium intake was associated with a 32% increase in stroke incidence, 89% increase in stroke mortality, 44% increase in coronary heart disease mortality, 61% increase in cardiovascular disease mortality, and 39% increase in mortality from all causes.

Interestingly dietary sodium intake was not significantly associated with cardiovascular disease risk in non-overweight persons.

The authors concluded that high sodium intake is associated with an increased risk of cardiovascular disease and all-cause mortality in overweight persons.

He J, Ogden LG, Vupputuri S, Bazzano LA, Loria C, Whelton PK. Dietary Sodium Intake and Subsequent Risk of Cardiovascular Disease in Overweight Adults. JAMA. 1999;282(21):2027–2034. doi:10.1001/jama.282.21.2027

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Detection and Treatment of Atherosclerosis Using Nanoparticles 

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Detection and Treatment of Atherosclerosis Using Nanoparticles 

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The key pathogenesis of cardiovascular disease is atherosclerosis. When I found this article, I was very impressed and research like this is the reason why I chose medicine for my career. Being the leading cause of death in the United States, we need a solution and we need a solution fast. Atherosclerosis is currently, in its early stages, difficult to detect with current methods and equipment. During the early stages, there are not many associated symptoms and it can go undetected until it’s too late, leading to myocardial infarctions or strokes. This study describes how we can use nanoparticles to help better detect atherosclerosis in its early stages of development to help better treat patients and prevent heart events. Nanoparticles have potential in improving atherosclerosis detection and treatment via targeting the intimal macrophages, foam cells, endothelial cells, angiogenesis, proteolysis, apoptosis, and thrombosis. They can engineer targeted delivery of diagnostic agents or therapeutic compounds to specific molecules, cells, or tissues. They have also shown an anti-inflammatory response.

The clinical implications of this study is that as technology and medicine advance, we will find innovative approaches to help better treat people that live with cardiovascular disease and atherosclerosis. I would argue most people are developing slight atherosclerosis with the current diet in the United States. If we could help detect atherosclerosis and its earlier stages, it could help save billions of dollars a year in healthcare costs and help people live better lives.

Stephen Mayer

Zhang, J., Zu, Y., Dhanasekara, C. S., Li, J., Wu, D., Fan, Z., & Wang, S. (2017). Detection and treatment of atherosclerosis using nanoparticles. Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology, 9(1), 10.1002/wnan.1412. https://doi.org/10.1002/wnan.1412

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Cassie Craig: Optimum nutritional strategies for cardiovascular disease prevention and rehabilitation

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Cassie Craig: Optimum nutritional strategies for cardiovascular disease prevention and rehabilitation

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This study is important because it emphasizes the importance of researching nutrition in cardiovascular disease as a treatment, as well as a preventative measure. The earlier those at-risk for CVD can address it in their diet, the better the outcome will be for the patient. This study focused on the importance of emphasizing whole foods/well-rounded diets to patients instead of just macronutrients. They addressed the constant development of nutritional sciences, and how that puts a strain on the patient. Focusing on the whole food makes it easier for patients to develop a diet, with the help of their physicians, that they can tailor to their specific needs. The clinical implications of this study include collaborations between physicians, dietitians, and the patient to develop a personalized diet that addresses CVD, as well as any other comorbidities the patient may be facing. Personalization of the diet makes it easier for the patient to follow it, in comparison to being told to increase or decrease specific macronutrients.

Butler, Tom & Kerley, Conor & Altieri, Nunzia & Alvarez, Joe & Green, Jane & Hinchliffe, Julie & Stanford, Dell & Paterson, Katherine. (2020). Optimum nutritional strategies for cardiovascular disease prevention and rehabilitation (BACPR). Heart. 106. heartjnl-2019. 10.1136/heartjnl-2019-315499.

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Smoking and Vascular risk: are all forms of smoking harmful to all types of vascular disease? 

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Smoking and Vascular risk: are all forms of smoking harmful to all types of vascular disease? 

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The study above examines various types of smoking including cannabis, cigar, pipe, smokeless tobacco, and cigarette smoking and their individual impact on cardiovascular risk. The study also looks at additional cardiovascular risk factors such as hypertension, diabetes, dyslipidaemia, and haemostasis and its correlation with smoking and smoking cessation. This is an important study because I believe the risks associated with all types of smoking should be explicitly stated. The study also compares the risk factors to one another. For example cigar smoking has a higher risk of non-fatal and fatal stroke compared to previous cigarette smokers. In addition to outlining the risk associated with each smoking form, the article examines the risks associated weight gain after smoking cessation. This is important as weight gain/obesity is a risk factor for cardiovascular disease. By knowing which forms of smoking could induce weight gain after cessation, people can take appropriate precautions as to not put themselves at higher risk. This could be ensuring that they follow a cardiovascular friendly diet such as the DASH diet or the mediterranean diet as they are in the process of smoking cessation. The study concluded that all smoking forms were harmful to vasculature, increasing risks for cardiovascular events.

N. Katsiki, S.K. Papadopoulou, A.I. Fachantidou, D.P. Mikhailidis,
Smoking and vascular risk: are all forms of smoking harmful to all types of vascular disease?,Public Health,Volume 127, Issue 5, 2013, Pages 435-441,
ISSN 0033-3506, https://doi.org/10.1016/j.puhe.2012.12.021.

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Eating Patterns and Cardiovascular Disease Risk in a Detroit Mexican American Population - Dierra Doaks 

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Eating Patterns and Cardiovascular Disease Risk in a Detroit Mexican American Population - Dierra Doaks 

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The article that I found for this week was very interesting. It was about the relationship between eating habits and cardiovascular disease risk in Mexican American adults living in Southwest Detroit. According to the article, cardiovascular disease is the leading cause of death in Mexican Americans and they have a higher prevalence rate of obesity compared to non-Hispanic White Americans. Obesity is a cardiovascular risk factor so this is essential to note. A study was done with 32 Mexican Americans who self reported data. The results of the study showed that unhealthy eating habits greatly outnumbered healthy eating habits. These eating habits included using higher fat salad dressings, eating fried foods, and eating high fat snacks. The study highlights Mexican American eating habits in this area that can impact the risk of cardiovascular disease. The article was important because it addresses the need for heart disease prevention programs at community levels and education on risk factor screenings.

Artinian, Nancy T et al. “Eating Patterns and Cardiovascular Disease Risk in a Detroit Mexican American Population.” Public health nursing (Boston, Mass.) 21.5 (2004): 425–434. Web.

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Dietary fat intake and risk of cardiovascular disease and all-cause mortality in a population at high risk of cardiovascular disease Post by Jaida Garrett

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Dietary fat intake and risk of cardiovascular disease and all-cause mortality in a population at high risk of cardiovascular disease Post by Jaida Garrett

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This article was very interesting and I really liked the further intent of research it provides. This is so important because this research tries to dive deeper into what fats actually help or induce cardiovascular disease (CVD). The study looks more into how monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA) lower the risk of CVD. A key finding is that instead of monitoring the amount of fat intake monitor the type of fat that is being taken in. So, in contrast to MUFA and PUFA you have saturated fats and trans fats. Saturated and trans fats are known to contribute the CVD and its risk factors. Specifically, though, saturated or trans fats from processed foods contribute to CVD; saturated fats in vegetables or fish contribute to a low risk of CVD. The clinical implication of this study is that it will greatly help physicians and dieticians with their patients. Instead of taking fat out of a person’s diet replace unhealthy fats with healthier fats in order to reduce risks for CVD and reduce adverse effects in individuals dealing with CVD.

PREDIMED Study Investigators, Dietary fat intake and risk of cardiovascular disease and all-cause mortality in a population at high risk of cardiovascular disease, The American Journal of Clinical Nutrition, Volume 102, Issue 6, December 2015, Pages 1563–1573, https://doi.org/10.3945/ajcn.115.116046

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Julie Rees - Nut Consumption and Risk of Cardiovascular Disease

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Julie Rees - Nut Consumption and Risk of Cardiovascular Disease

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We have long been told that eating nuts is beneficial to our health.  This longitudinal study looked not only at total nut consumption but also looked at specific nuts and nut products.  They found that those who consumed nuts had a significantly reduced risk of cardiovascular disease, particularly coronary heart disease, based on the number of fatal and nonfatal myocardial infarctions, but no significant reduction in stroke risk.  There was a significant reduction in CV events in those that ate whole nuts like peanuts and tree nuts.  The greatest reduction was in those who consumed walnuts.  There was no difference in those who consumed peanut butter.  This may be linked to other dietary choices made by those who eat peanut butter on a regular basis.  We know that patients are more successful when they can make simple, gradual changes to their diets.  Replacing three snacks a week with walnuts  could potentially reduce the risk of a CV event in the patient.

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J Am Coll Cardiol. Author manuscript; available in PMC 2018 Nov 14.

Published in final edited form as:

Marta Guasch-Ferré, PhD, a Xiaoran Liu, PhD, a Vasanti S Malik, PhD, a, b Qi Sun, MD, ScD, a, b Walter C Willett, MD, DrPH, a, b, c JoAnn E Manson, MD, DrPH, c, d Kathryn M Rexrode, MD, MPH, c, d Yanping Li, MD, PhD, a Frank B Hu, MD, PhD, a, b, c and Shilpa N Bhupathiraju, PhD a, b

Abstract

Background

The associations between specific types of nuts, specifically peanuts and walnuts, and cardiovascular disease remains unclear.

Objectives

To analyze the associations between the intake of total and specific types of nuts and cardiovascular disease, coronary heart disease, and stroke risk.

Methods

We included 76,364 women from the Nurses' Health Study (1980-2012), 92,946 women from the Nurses' Health Study II (1991-2013), and 41,526 men from the Health Professionals Follow-up Study (1986-2012) who were free of cancer, heart disease, and stroke at baseline. Nut consumption was assessed using food frequency questionnaires at baseline and updated every 4 years.

Results

During 5,063,439 person-years of follow-up, we documented 14,136 incident cardiovascular disease cases, including 8,390 coronary heart disease cases and 5,910 stroke cases. Total nut consumption was inversely associated with total cardiovascular disease and coronary heart disease after adjustment for cardiovascular risk factors. The pooled multivariable hazard ratios for cardiovascular disease and coronary heart disease among participants who consumed one serving of nuts (28 g) five or more times per week, compared to the reference category (never or almost never), were 0.86 [95% confidence interval (CI), 0.79-0.93, P trend 0.0002] and 0.80 [95% CI, 0.72-0.89, P trend <0.001], respectively. Consumption of peanuts and tree nuts (two or more times/week) and walnuts (one or more times/week), was associated with a 13%-19% lower risk of total cardiovascular disease and 15-23% lower risk of coronary heart disease.

Conclusions

In 3 large prospective cohort studies, higher consumption of total and specific types of nuts was inversely associated with total cardiovascular disease and coronary heart disease.

Keywords: Nuts, cardiovascular disease, coronary heart disease, stroke, peanuts, tree nuts

Introduction

Cardiovascular disease (CVD) remains a leading cause of death worldwide and hence prevention of CVD has become a top public health priority ( 1). In recent years, dietary recommendations have shifted towards diets high in plant-based foods and low in animal-based foods for the prevention of chronic diseases ( 2). Most of these plant-based dietary patterns highlight the intake of nuts as a key component. Nuts have a unique nutritional composition ( 3) and are good sources of unsaturated fatty acids, dietary fiber, minerals, vitamins, and other bioactive compounds ( 4).

Frequent nut consumption has been associated with reduced cardiovascular risk factors including dyslipidaemia, type 2 diabetes and metabolic syndrome; as well as with lower risk of coronary heart disease (CHD) ( 5- 8). Findings from prospective cohort studies were confirmed by a randomized primary-prevention trial conducted in a Mediterranean population at high cardiovascular risk ( 9). Participants randomized to a Mediterranean diet supplemented with mixed nuts-hazelnuts, almonds, and walnuts-had a 28% reduction in the incidence of major cardiovascular events after about 5 years of follow-up ( 9). Recent findings from the Nurses' Health Study (NHS) and the Health Professionals Follow-up Study (HPFS) have also provided further evidence that the frequency of nut consumption is inversely associated with total and cause-specific mortality ( 10).

Most of the previous prospective studies have focused on total nut consumption in relation to the risk of CVD ( 11, 12). However, the associations between peanut butter and specific types of nuts, such as peanuts and walnuts, with major cardiovascular events, and specifically the relation with stroke remain unclear. Of note, because the nutritional composition of peanuts and walnuts differs from other nuts ( 13), evaluating the health effects of specific types of nuts is of particular interest.

Our primary hypothesis is that frequent nut consumption is associated with lower risk of CVD incidence. Therefore, we examined the associations between the intake of total and specific types of nuts with CVD in three large prospective cohort studies. Our cohorts provided repeated measures of diet (including separate data on peanuts, walnuts, tree nuts, and peanut butter), extensive data on cardiovascular risk factors, up to 32 years of follow-up, and a large number of incident CVD cases.

Methods

Study population

The NHS is a prospective cohort study of 121,700 female nurses, aged 30 to 55 years, from 11 U.S. states that began in 1976. The NHS II was established in 1989 and consists of 116,671 younger female registered nurses, aged 25 to 42 years at baseline. The HPFS is a prospective cohort study of 51,529 male health professionals aged 40 to 75 years at baseline that began in 1986. In all three cohorts, information about medical history, lifestyle, and health conditions has been collected by self-administered questionnaires every two years since baseline. Detailed information on the cohorts has been described previously elsewhere ( 14- 16).

For the present analysis, baseline year was defined as the first year when the validated food-frequency questionnaire (FFQ) was collected in each study-1980 for the NHS, 1991 for NHS II, and 1986 for HPFS. We excluded from the analysis those participants who reported CVD or cancer at baseline, participants who did not provide information on nut consumption, those who left more than 70 food items blank in the FFQ, or had daily energy intakes <600 or >3500 kcal for women and <800 or >4200 kcal for men. The final analyses included 76,364 women in the NHS, 92,946 women in the NHS II and 41,526 men in the HPFS. The institutional review boards of Brigham and Women's Hospital and Harvard T.H. Chan School of Public Health approved the study protocol.

Ascertainment of CVD

Our primary outcome measure was major CVD defined as a combined endpoint of myocardial infarction, stroke, or fatal CVD (fatal stroke, fatal myocardial infarction, and CV death). We further assessed the following secondary outcome measures: total CHD, which was defined as fatal or non-fatal myocardial infarction; and total stroke, which included all fatal and non-fatal stroke cases (ischemic, hemorrhagic, and undetermined subtypes). When a participant (or family members of deceased participants) reported an incident event, permission was requested to examine their medical records by physicians who were blinded to participant risk factor status. For each endpoint, the month and year of diagnosis were recorded as the diagnosis date. Nonfatal events were confirmed through review of medical record by study investigators blinded to participant risk factor status. Myocardial infarction was confirmed if the World Health Organization criteria were met based on symptoms plus diagnostic electrocardiogram changes or elevated cardiac enzymes ( 17). If medical records were unavailable, we considered myocardial infarctions probable when the participant provided additional confirmatory information. Information on angina and coronary revascularization procedures (percutaneous transluminal coronary angioplasty or coronary artery bypass grafting surgery) was self-reported, and we included only events that occurred before a manifest cardiovascular event.

Strokes were confirmed if data in the medical records fulfilled the National Survey of Stroke criteria requiring evidence of a neurologic deficit with sudden or rapid onset that persisted for >24 hours or until death ( 18). We excluded cerebrovascular pathology due to infection, trauma, or malignancy, as well as "silent" strokes discovered only by radiologic imaging. Radiology reports of brain imaging (computed tomography or magnetic resonance imaging) were available in 89% of those with medical records. We classified strokes as ischemic stroke (thrombotic or embolic occlusion of a cerebral artery), hemorrhagic stroke (subarachnoid and intraparenchymal hemorrhage), or stroke of probable/unknown subtype (a stroke was documented but the subtype could not be ascertained owing to medical records being unobtainable).

Deaths were identified by reports of families, the U.S. postal system, or using death certificates obtained from state vital statistics departments and the National Death Index and confirmed through review of medical records or autopsy reports. Follow-up for deaths was >98% complete ( 19). Fatal CVD was defined as fatal CHD disease, fatal stroke, or fatal CVD. Fatal CHD was defined as ICD-9 (international classification of diseases, ninth revision) codes 410-412 and was considered confirmed if fatal CHD was confirmed via medical records or autopsy reports or if CHD was listed as the cause of death on the death certificate and there was prior evidence of CHD in the medical records. We designated as probable those cases in which CHD was the underlying cause on the death certificates but no prior knowledge of CHD was indicated and medical records concerning the death were unavailable. Similarly, we used ICD-9 codes 430-434 to define fatal stroke and followed the same procedures to classify cases of confirmed or probable fatal stroke. Lastly, fatal CVD was defined by ICD-9 codes 390-458.

Dietary assessment

A semi-quantitative food-frequency questionnaire with over 130 items administered every 2 to 4 years was used to assess dietary intake. In the 1980 and 1984 dietary questionnaires, we asked participants how often they had consumed a serving of nuts (serving size, 28 g [1 oz]) during the preceding year: never or almost never, one to three times a month, once a week, two to four times a week, five or six times a week, once a day, two or three times a day, four to six times a day, or more than six times a day. In subsequent food-frequency questionnaires, the question regarding nuts was split into two items: peanuts and other nuts. A specific question about walnut consumption was first introduced on the questionnaires in 1998 in the NHS and HPFS and 1999 in the NHS II. Total nut consumption was defined as the intake of peanuts, other nuts, and walnuts (if available). Intake of peanut and peanut butter or other forms of peanuts was assessed and analyzed separately in the current analysis. Tree nuts included all types of tree nuts including walnuts (not including peanuts, which are botanically a legume but with a similar fatty acid and nutrient profile as other nuts). Consumption of peanut butter was assessed in 1980, 1984, 1986, 1990, and 1994, with the same 9 responses as those for nut consumption (serving size, 15 g [1 tablespoon]). A validation study indicated that nut consumption was reported with reasonable accuracy; the corrected coefficient was 0.75 between the FFQ and four 1-week diet record for total nuts and peanut butter ( 20).

Statistical analysis

We calculated each individual's person-time from the date of the return of the baseline questionnaire to the date of death or the end of follow-up (June 2012 in NHS, June 2013 in NHSII and January 2012 in HPFS), whichever comes first. The cumulative average of nut consumption was calculated to better represent long-term diet and to minimize within-person variation. We stopped updating dietary variables on a report of cancer, coronary artery bypass, or angina because changes in diet after development of these conditions may confound the relation between diet and chronic diseases.

We used Cox proportional-hazards regression models to estimate hazard ratios and 95% confidence intervals of developing total CVD, CHD, and stroke according to nut consumption categories. Separate analyses were conducted for fatal and nonfatal CVD, nonfatal myocardial infarction, fatal CHD, fatal and nonfatal stroke, and ischemic stroke. We did not analyze hemorrhagic stroke separately due to the lower number of cases. Multivariable models were adjusted for updated over time covariates: age (continuous); Caucasian (yes/no); body-mass index (<23, 23-24.9, 25-29.9, 30-34.9, ≥35 kg/m2); physical activity (metabolic-equivalents/week, quintiles); smoking status (never, past, current 1-14 cigarettes/d, current 15-24 cigarettes/d, current ≥25 cigarettes/d); physical examination for screening purposes (yes/no); current multivitamin use(yes/no); and current aspirin use (yes/no); family history of diabetes mellitus (yes/no), myocardial infarction (yes/no), or cancer (yes/no); history of diabetes mellitus (yes/no), hypertension (yes/no), or hypercholesterolemia (yes/no); intakes of total energy (kcal/d), alcohol (g/d), red or processed meat (servings/d), fruits (servings/d), and vegetables (servings/d) (all in quintiles); and, in women, menopausal status and hormone use (premenopausal, postmenopausal never users, postmenopausal past users, postmenopausal current users). In NHS II, the multivariable model was further adjusted for oral contraceptive use (never, past and current users). The above covariates were updated every 2 or 4 y using the most recent data for each 2-y follow-up interval. P values for trend were calculated with the use of the Wald test of a continuous variable based on the median number of servings of nuts consumed per day for each category.

We performed separate analyses for peanuts, tree nuts, walnuts, and peanut butter intake. Peanut butter models were additionally adjusted for quintiles of glycemic load, white bread, and soda intake, to control for dietary components associated with the consumption of peanut butter. For these analyses, we combined categories of high nut intake (≥2 servings/week) to maintain statistical power. We also analyzed nuts and types of nuts as a continuous variable (per 1 serving (28g) increase).

We conducted several sensitivity analyses to test the robustness of the results. First, we conducted pre-specified subgroup analyses by potential effect modifiers and the interaction between nut intake and covariates was examined using the likelihood-ratio test. Second, to test if our results were biased by selectively stopping updating diet after an intermediate outcome, we continuously updated diet until the end of follow-up. Third, instead of using repeated measures of diet, we used the most recent measure of diet. Fourth, we analyzed the association between baseline nut consumption and the incidence of CVD, CHD and stroke. Fifth, we further adjusted the models for the number of natural teeth (0-10, 11-16, 17-32 teeth) in NHS and HPFS, where the information was available, as tooth loss may be a marker for periodontal disease, which has been shown to be previously associated with CVD risk ( 21). Sixth, we further adjusted the models for the Alternate Healthy Eating Index (AHEI) ( 22), excluding the nut component. For the analysis including specific types of nuts, we mutually adjusted for other types of nuts (i.e., peanuts mutually adjusted for tree nuts and peanut butter). Finally, we conducted sensitivity analysis excluding BMI from the models.

The hazard ratios from multivariable models in each cohort were pooled with the use of an inverse variance-weighted meta-analysis using a fixed-effects model. P values for heterogeneity were calculated with the use of the Q statistics. Analyses were performed with the SAS statistical package (version 9.4, SAS institute). Statistical tests were two sided, and P values of less than 0.05 were considered to indicate statistical significance.

Results

During an average of 28.7 years of follow-up in the NHS, 21.5 years in the NHS II, and 22.5 years in the HPFS (and a total of 5,063,439 person-years across the three cohorts), we documented 14,136 incident CVD cases, including 8,390 CHD and 5,910 stroke cases. Compared to those participants who never or almost never consumed nuts, those who consumed nuts more frequently were older, had a lower BMI, were less likely to smoke, more likely to exercise, and consumed more fruits and vegetables ( Table 1 ). Participants' characteristics according to the frequency of peanut and walnut consumption are shown in Online Tables 1 and 2, respectively. Online Table 3 shows the Pearson correlations among different types of nuts in the three cohorts.

Table 1

Frequency of Nut Consumption

Characteristics

Never or almost never

Less than once per week

Once per week

Two to four times per week

Five or more times per week

BMI (kg/m ²)

26.1(5.4)

26.1(5.2)

25.8(5.0)

25.4(4.8)

25.0(4.8)

BMI (kg/m ²)

26.8(6.4)

26.8(6.3)

26.4(6.2)

25.8(6.0)

25.2(5.7)

BMI (kg/m ²)

25.7(3.5)

26.0(3.5)

26.0(3.5)

25.9(3.6)

25.5(3.4)

Age-adjusted and multivariable-adjusted analyses showed a consistent significant inverse association between total nut consumption and total CVD and CHD ( Table 2 ). The pooled multivariable hazard ratios, without heterogeneity by sex or cohort, for those who consumed nuts five or more times per week (1 serving of nuts = 28g), as compared with those who never consumed nuts, were 0.86 (95% confidence interval [CI], 0.79-0.93, P<0.001) for total CVD and 0.80 (95% CI, 0.72-0.89, P<0.001) for CHD. Each serving increase of nuts was associated with 6% [HR: 0.94; 95% CI, 0.89-0.99)] and 13% [HR: 0.87; 95% CI, 0.81-0.94)] lower risk of CVD and CHD, respectively. Total nut consumption was inversely associated with both fatal [HR:0.76; 95% CI, 0.70-0.84, P=0.0003] and nonfatal CVD [HR:0.91; 95% CI, 0.85-0.98, P=0.005] in the pooled analysis of the three cohorts ( Online Table 4).

Table 2

Frequency of Nut Consumption

Never or almost never

Less than once per week

Once per week

Two to four times per week

Five or more Times per week

P value for trend

HR (95% CI) per 28 g increase

TOTAL CARDIOVASCULAR DISEASE: fatal and nonfatal myocardial infarction + fatal and nonfatal stroke

Pooled*
Multivariable-adjusted

1

0.91 (0.86-0.95)

0.90 (0.85-0.95)

0.86 (0.81-0.91)

0.86 (0.79-0.93)

0.0002

0.94 (0.89-0.99)

CORONARY HEART DISEASE: fatal and nonfatal myocardial infarction

Pooled*
Multivariable-adjusted

1 (Ref.)

0.88 (0.83-0.94)

0.83 (0.78-0.90)

0.82 (0.76-0.88)

0.80 (0.72-0.89)

<0.0001

0.87 (0.81-0.94)

STROKE: fatal and nonfatal stroke

Pooled*
Multivariable-adjusted

1 (Ref.)

0.95 (0.88-1.03)

1.01 (0.92-1.10)

0.95 (0.87-1.04)

0.98 (0.86-1.13)

0.88

1.02 (0.96-1.08)

In separate analyses of specific types of nuts ( Central Illustration , Table 3 ), when comparing consumption of nuts two or more times per week with the reference category, the pooled multivariable-adjusted hazard ratios for CVD were 0.87 (95% CI, 0.82-0.93) for peanuts, and 0.85 (95% CI, 0.79-0.91) for tree nuts. Consuming walnuts one or more times per week was also associated with a lower risk of CVD [HR: 0.81 (95% CI, 0.71-0.91)]. Significant associations were also observed for each serving increase in peanuts, tree nuts and walnuts. Peanut butter intake was not significantly associated with CVD. Significant inverse associations were observed between the intake of total nuts, peanuts, tree nuts, and walnuts and CHD risk ( Central Illustration , Online Table 5). Participants who consumed peanuts or tree nuts two or more times per week had respectively 15% (95% CI 8-21%) and 23% (95% CI 16-30%) lower risk of CHD compared to those who never or almost never consumed nuts. Consuming walnuts one or more times per week was associated with 21% (95% CI 6-34%) lower risk of CHD. Pooled analyses of the three cohorts showed that total nut consumption was inversely associated with fatal CHD [HR:0.69; 95% CI, 0.61-0.77, P<0.0001] but non-significant associations were observed for nonfatal myocardial infarction ( Online Table 6).

Table 3

Frequency of Nut Consumption

Never or almost never

Less than once per Week

Once per Week

Two or more times per Week

P value for trend

HR (95% CI) per 28 g increase

Peanuts

Tree nuts

Walnuts

Peanut butter

Peanuts

Tree nuts

Walnuts

Peanut butter

Peanuts

Tree nuts

Walnuts

Peanut butter

Pooled*

Peanuts

Tree nuts

Walnuts

Peanut butter

The pooled risk estimates for stroke among participants who consumed total nuts and peanuts two or more times per week was 0.94 (95% CI, 0.88-1.05, P=0.08) and 0.90 (95% CI, 0.81-0.99, P=0.07), respectively. Walnut intake was associated with a 17% (95% CI, 4%-29%, P=0.10) lower risk of stroke ( Central Illustration , Online Table 5). Peanut butter and tree nuts were not associated with stroke risk ( Online Table 5). Likewise, we found no significant associations between total nut consumption and the risk of fatal, nonfatal or ischemic stroke ( Online Table 7).

In analyses stratified by potential risk factors for CVD, the inverse association between total nut consumption and CVD persisted in most subgroups ( Figure 1 ). No significant interactions were observed in pooled analysis. Our results remained robust in several sensitivity analyses. The results remained unchanged when we continuously updated diet until the end of follow-up (pooled multivariable HR for CVD comparing nut consumption five or more times per week with no nut consumption: HR: 0.86, 95% CI, 0.78-0.94, P<0.001) and when we used the most recent diet as our primary exposure (pooled multivariable HR for CVD comparing nut consumption five or more times per week with no nut consumption: HR: 0.88 (95% CI, 0.82-0.94 P<0.001). Additional adjustment for tooth loss or AHEI (excluding nut component) did not materially alter the associations (data not shown). When specific types of nuts were mutually adjusted for other nuts in individual cohorts, results were attenuated (i.e. peanuts mutually adjusted for tree nuts and peanut butter). However, significant inverse associations remained in the pooled analysis for peanuts and tree nuts ( Online Table 8). Significant inverse associations between baseline nut consumption and risk of CVD and CHD were also observed ( Online Table 9). Results were consistent with primary analysis when we excluded BMI from the multivariable adjusted model (pooled multivariable HR for CVD comparing nut consumption five or more times per week with no nut consumption: HR: 0.85 (95% CI, 0.79-0.93 P<0.001).

Discussion

In three large prospective cohorts with up to 32 years of follow-up, we observed that nut consumption was associated with lower risk of developing CVD after adjusting for cardiovascular risk factors. As compared to those participants who never or almost never consume nuts, those who consumed nuts five or more times per week had 14% lower risk of CVD and 20% lower risk of CHD. Results were similar for tree nuts, peanuts, and walnuts; and the inverse association persisted across all subgroups in stratified analysis. Significant inverse associations were observed for each increasing serving of nuts and risk of CVD and CHD. Although we found no evidence of an association between total nut consumption and risk of stroke, the intake of peanuts and walnuts was inversely associated with the risk of stroke.

Our results are in line with previous observational studies that reported inverse associations between nut consumption and CVD risk. However, the number of studies that investigated specific types of nuts is limited and few of them had repeated measures of diet ( 11, 12). To date, twelve cohort studies have investigated the association between total nut consumption and CVD risk ( 11). Consistent with our findings, a recent meta-analysis of these twelve studies found a summary relative risk for high versus low intake of nuts of 0.81 (95 % CI: 0.74-0.89) for CVD and 0.76 (95% CI: 0.69-0.84) for CHD ( 11). Our results are in agreement with a meta-analysis of 7 prospective studies that showed a 30% lower risk of CHD mortality in participants with higher nut consumption and no significant associations for non-fatal CHD, but only 3 studies examined nut consumption in relation to non-fatal CHD ( 12).

Despite studies reporting consistent inverse associations between higher nut consumption and risk of CVD and CHD, studies evaluating associations with stroke remain limited ( 11). In the pooled analysis of our cohorts, we found that consumption of peanuts two or more times per week and walnuts one or more times per week was associated with a 10% and 17% lower risk of total stroke, respectively, but there was no significant associations for total nut intake. In a meta-analysis of eleven prospective studies, an inverse association was observed for total nut consumption and total stroke risk [HR: 0.89 (95% CI: 0.82-0.97) for high vs. low intake] ( 11). However, the associations were not significant in eight of the individual studies included, and most of the studies did not differentiate between fatal and nonfatal stroke. Two studies evaluated the associations between intake of specific types of nuts and stroke death. The Shanghai Men's Health Study ( 23) reported an inverse trend between higher peanut intake and lower risk of ischemic stroke (HR comparing 5th versus 1st quintile = 0.77 (0.60-1.00), P-trend=0.003). In the Netherlands Cohort Study ( 24), an intake of more than 5 g/d of peanuts was associated with a 29% (6-46%) lower risk of stroke death compared to those who did not consume peanuts. Another reason that may account for the lack of associations between nut intake and stroke, is the lack of effect of nuts on blood pressure ( 25).

Walnuts are among the most widely consumed tree nut in the world and are high in n-6 and n-3 PUFA (especially in plant-derived α-linolenic acid). Their consumption has been associated with cardio protective properties ( 26). Although numerous clinical studies have shown beneficial effects of walnuts on lipid profiles and inflammatory biomarkers ( 27), evidence from large prospective studies with long durations of follow-up is sparse. In a secondary analysis of the PREDIMED trial, participants who consumed >3 servings per week of walnuts had 47% (2% to 71%) lower risk of cardiovascular mortality compared to those who did not consume walnuts ( 28). We have also observed that consuming walnuts at least once per week was associated with 19% lower risk of CVD, 21% lower risk of CHD and 17% lower risk of stroke.

Peanut butter intake was inversely associated with CVD and stroke in the NHS II but no significant associations were observed when pooling the three cohort studies together. Although we conducted several sensitivity analyses adjusting peanut butter models for foods associated with peanut butter consumption (such as soda, white bread, and glycaemic load), residual confounding by dietary pattern remains a strong possibility. Further, it may be possible that peanut butter intake is not associated with disease risk. In a previous report of the NHS and HPFS, peanut butter intake was not associated with inflammatory biomarkers ( 29). Of note, in our cohorts, a serving of peanut butter was defined as 1 tablespoon (15 g), which is not consistent with the typical serving size of 2 tablespoons and may have misclassified intake levels. Further studies are needed to elucidate the health effects of peanut butter intake.

Findings from observational studies alone cannot be used to draw conclusions regarding whether associations are causal, however, the PREDIMED trial found that participants who were randomized to a Mediterranean diet supplemented with mixed nuts had 28% (95% 0.54-0.96) reduced risk of a composite of cardiovascular events and 46% (95% CI, 0.35-0.84) reduced risk of stroke after 4.8 years of follow-up compared to a control diet (advice to reduce all types of dietary fat) ( 9).

Nuts are high in unsaturated fatty acids, dietary fiber, minerals, vitamins and several bioactive compounds, which may in part explain their beneficial effects on cardiovascular health ( 30). There are several mechanisms that may account for the inverse associations between nut consumption and CVD. Randomized controlled trials have shown that consumption of nuts improves lipid profiles ( 5, 27), attenuate inflammation ( 31), oxidative stress and endothelial function ( 32), and decreases insulin resistance ( 33). Nuts are also rich in polymerized polyphenols which provide a substrate for gut microbiota. The compounds arising from this metabolism may modulate gut microbiota through prebiotic effects and antimicrobial activities and consequently contribute to cardiovascular benefits for the host ( 34). Despite nuts being an energy-dense food, there is no scientific evidence supporting associations between weight gain and nut consumption. Indeed, they have been associated with lower weight gain and lower risk of obesity, probably because they can increase satiety and fullness which may potentially reduce the consumption of unhealthy snacks ( 35 -37).

The strengths of the present study include its prospective design, large sample size including men and women, long duration of follow-up with a high retention rate, repeated assessment of diet and lifestyle variables, and analyses of several CVD outcomes including fatal and nonfatal CVD, fatal and nonfatal CHD, and stroke (fatal, nonfatal and ischemic). Moreover, we present strong evidence for the association between total nuts, peanuts, tree nuts, walnuts and peanut butter with CVD risk in three large cohort studies with more than 13,500 CVD cases. Several limitations deserve comment. First, given that our study sample was limited to white health professionals, this could limit generalizability of our findings. Still, because there is no reason to expect that the underlying biological mechanisms may be different, our results can be generalized to men and women of different ethnicities. Because nut intake was self-reported, some measurement error is inevitable. However, because dietary data were collected prospectively, misreporting is likely to be random, resulting in an underestimation of the association. By calculating the cumulative average of nut intake from multiple time points, we were able to reduce potential random measurement error. Further, inverse associations were consistent across pre-specified subgroup analysis and in several sensitivity analyses. Because we lacked data on how nuts were prepared (e.g., salted, raw, roasted), we were unable to test the influence of preparation methods.

In conclusion, findings from three large prospective cohort studies indicate that frequent intake of nuts, tree nuts, peanuts and walnuts was associated with a lower risk of CVD, independently from other cardiovascular risk, lifestyle, and dietary factors. Our findings support recommendations of increasing the intake of a variety of nuts, as part of healthy dietary patterns, to reduce the risk of chronic diseases in the general population.

​

Competency in Medical Knowledge

Consumption of peanuts and tree nuts two or more times per week and walnuts one or more times/week is associated with a lower risk of coronary artery disease and cardiovascular disease in general.

Competency in Patient Care

Increasing intake of nuts, as part of a healthy diet, may help to reduce the risk of cardiovascular disease in the general population.

Translational Outlook

Further research is needed to investigate the mechanisms underlying the association between nut consumption and reduction in cardiovascular risk.

Acknowledgments

Funding: This study was supported by research grants UM1 CA186107, R01 HL034594, R01 HL088521, UM1 CA176726, UM1 CA167552, R01 HL35464, R01 HL60712 from the National Institutes of Health, United States. SNB is supported by a Career Development Grant from the National Institutes of Health (K01 DK107804).

We thank the participants and staff of the Nurses' Health Study, Nurses' Health Study II, and Health Professionals Follow-up Study for their valuable contributions.

Abbreviations

CHD

coronary heart disease

CI

confidence interval

CVD

cardiovascular disease

FFQ

food frequency

HPFS

Health Professionals Follow-up study

HR

hazard ratio

NHS

Nurses' Health Study

US

United States

Footnotes

Disclosures: Drs. Yanping Li and Frank Hu have received research support from California Walnut Commission. Dr. Vasanti Malik has received research support from the Peanut Institute. Neither the corresponding author nor other authors have any conflict of interest affecting the conduct or reporting of the work submitted.

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

References

2. U.S. Department of Agriculture and U.S. Department of Helath and Human Services. Scientific Report of the 2015 Dietary Guidelines Advisory Committee. 2015 [ Google Scholar]

36. Freisling H, Noh H, Slimani N, et al. Nut intake and 5-year changes in body weight and obesity risk in adults: results from the EPIC-PANACEA study. Eur J Nutr. 2017 In press. [[ PubMed] Google Scholar]

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Nut Consumption and Risk of Cardiovascular Disease

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J Am Coll Cardiol. Author manuscript; available in PMC 2018 Nov 14.

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Kate Mashburn - Dyslipidemia influences the effect of physical exercise on inflammatory markers on obese women in post-menopause: A randomized clinical trial

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Kate Mashburn - Dyslipidemia influences the effect of physical exercise on inflammatory markers on obese women in post-menopause: A randomized clinical trial

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Many of the studies that I have found throughout these modules relate obesity to the diseases that we are studying. I think that just emphasizes how taking better care of your physical health can greatly reduce your chances of developing these conditions in the long run and can also minimize the symptoms associated with the disease. In this study, post-menopausal women who were obese and had dyslipidemia were evaluated on how physical exercise caused their symptoms to worsen or lessen. It was shown that frequent exercise greatly reduced symptoms and improved their overall quality of life. In most cases, their inflammatory markers were positively impacted, and they showed signs of improvement. Studies like this one are so important to give scientific evidence of how good exercise is to improve all aspects of health no matter what stage of life a person is in. I am sure this study was very impactful for the community of people living with dyslipidemia.

Biteli P, Barbalho SM, Detregiachi CRP, Dos Santos Haber JF, Chagas EFB. Dyslipidemia influences the effect of physical exercise on inflammatory markers on obese women in post-menopause: A randomized clinical trial. Exp Gerontol. 2021 Jul 15;150:111355. doi: 10.1016/j.exger.2021.111355. Epub 2021 Apr 15. PMID: 33865923.

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Nutrition and Atherosclerosis - Cole Zetter

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Nutrition and Atherosclerosis - Cole Zetter

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For this week's weekly wall I found an article titled "Nutrition and Atherosclerosis" I found this study to be important because it identified that cardiovascular disease is a universal problem in modern society also noting that atherosclerosis is the leading cause of cardiovascular disease resulting in high rate of mortality in the population. This is a serious issue. The study also noted how healthy lifestyle habits and nutritional habits are important to maintain to prevent atherosclerosis. Here, atherosclerosis is defined as an inflammatory disease that involves the arterial wall and is characterized by the progressive accumulation of lipids and inflammatory cells within the intima of large arteries. Throughout this article, key findings regarding nutrition were presented. For example, low magnesium levels in the blood and dietary magnesium intake correlate with an increase risk in cardiovascular disease in middle aged adults. This is important because magnesium has been found to play a critical role in modulating vascular smooth muscle tone, endothelial cell function, and myocardial excitability. Not only was magnesium mentioned, but many other vitamins and minerals were brought up and explained as to how their presence in the diet is important to preventing atherosclerosis. The clinical implications of this study would be to note the importance of a wide variety of nutrients, vitamins and minerals that can be found in the diet. It's important to maintain a healthy diet with a variety of nutrients to prevent plaque formation in the arteries. Nutrients such as saturated fatty acid and trans-fatty acids are associated with an increase in the development of atherosclerosis.

Torres, Nimbe et al. “Nutrition and Atherosclerosis.” Archives of medical research 46.5 (2015): 408–426. Web.

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Sidney Harm: Atherosclerosis imaging methods: assessing cardiovascular disease and evaluating the role of estrogen in the prevention of atherosclerosis

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Sidney Harm: Atherosclerosis imaging methods: assessing cardiovascular disease and evaluating the role of estrogen in the prevention of atherosclerosis

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This article discusses the imaging techniques used to help identify the progression of atherosclerosis. The most commonly used imaging technique to measure atherosclerosis is “serial coronary angiography” however this technique is hard to use for early state atherosclerosis before physical damage is done. This is important within nutritional sciences because these are imaging techniques that can be used to see how intervention techniques impacts the progression of atherosclerosis.

This article also discussed multiple trials used to determine estrogens effects on atherosclerosis. The Estrogen Replacement and Atherosclerosis Trial (ERA) investigated the effects of oral conjugated equine estrogen (0.625 mg) in addition to medroxyprogesterone acetate (2.5 mg). The sample included 309 women postmenopausal with CAD. In result of this study there was no found significance between the treatment groups, indicating estrogen doesn’t have an effect on CAD or atherosclerosis progression1.

In conclusion there are ways to keep track of the progression of atherosclerosis, there should be more studies based on nutritional treatments rather than your typical calorie restriction and increase of exercise.

References:
1. Hodis, & Mack, W. J. (2002). Atherosclerosis imaging methods: assessing cardiovascular disease and evaluating the role of estrogen in the prevention of atherosclerosis. The American Journal of Cardiology, 89(12), 19–27. https://doi.org/10.1016/S0002-9149(02)02407-4

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The Relationship Between Nutrition and Atherosclerosis 

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The Relationship Between Nutrition and Atherosclerosis 

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Ellen Reusch

For this week’s weekly wall, I found this article published in 2021 about nutrition and atherosclerosis. These researchers evaluated the relationship between atherosclerosis and phytosterols, omega-3 fatty acids, polyphenol, and vitamins. All of these nutritional elements can contribute, whether directly or indirectly, to the reduction of inflammation and oxidative stress within the body, which subsequently leads to a reduced risk of developing atherosclerosis. The study went even further to break down the ways each individual nutritional component can reduce this risk, such as by decreasing platelet stability, inhibiting leukocyte migration, or decreasing LDLs. Since the nutritional components evaluated in this article can all be increased in someone’s daily diet, and can be done so relatively easily, this article provides a lot of useful information for patients and providers to use to better manage their atherosclerosis or to decrease their risk for developing atherosclerosis.

Citation: Wei, et al., The Relationship Between Nutrition and Atherosclerosis. Frontiers in Bioengineering and Biotechnology. April 2021. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8094392/pdf/fbioe-09-635504.pdf

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Validation of the high mortality rate of Malnutrition-Inflammation-Atherosclerosis syndrome–Community-based observational study. Rhoda Inimgba.

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Validation of the high mortality rate of Malnutrition-Inflammation-Atherosclerosis syndrome–Community-based observational study. Rhoda Inimgba.

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The purpose of this paper was to investigate the relationship between malnutrition inflammation atherosclerosis (MIA) syndrome and high mortality rate of hemodialysis patients. This is important because inflammation has been seen in hemodialysis patients and also when atherosclerosis gets worse. Afterwards, inflammation can bring about malnutrition. Inflammation increases the levels of C-reactive proteins which serves as a risk factor of cardiovascular diseases.
A key finding of this study was that the high mortality rate of hemodialysis was directly proportional to the increased MIA factors which are malnutrition, inflammation and atherosclerosis. This relates to nutritional sciences as inflammation occurs, a person will not be able to take in more food which leads to malnourishment and thereby cause atherosclerosis.
The clinical implications is that if these three MIA factors are detected early in hemodialysis patients then the mortality rate can then be reduced which can lead to a better quality of life. This becomes very important especially in places where kidney transplantations are not done.

Sueta, Hokimoto, S., Sakamoto, K., Akasaka, T., Tabata, N., Kaikita, K., Honda, O., Naruse, M., & Ogawa, H. (2017). Validation of the high mortality rate of Malnutrition-Inflammation-Atherosclerosis syndrome: –Community-based observational study. International Journal of Cardiology, 230, 97–102. https://doi.org/10.1016/j.ijcard.2016.12.072.

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The purpose of the article was to identify the harmful or potentially harmful contents in water pipe smoke or hookah and to review the potential risk it poses to cardiovascular health. Smoking as discussed in the article and the lecture video plays a major role in prevalence and progression of cardiovascular disease. Surprisingly, hookah smoking is increasing globally, especially among youth and young adults. This may be because the social media environment advertises it as a healthier tobacco alternative. These misperceptions are proven to be false after one looks at the toxicological contents of hookah smoke   which include nicotine, carbon monoxide, particulates, oxidants, which all indicate a potential risk to cardiovascular disease. This relates to nutritional sciences as the evidence found within the article leads us to believe that the contents of hookah smoke contain similar chemicals found in cigarette smoke, then they will share the same harmful effects to cardiovascular health, such as problems with heart rate, blood pressure, tissue oxygenation, and coronary artery disease. The clinical implications of the article would be to offer guidance to healthcare providers and clinical dietitians for the identification and treatment of individuals who smoke tobacco using water pipes and also current research that are present especially concerning the cardiovascular consequences of hookah smoking, such as long-term issues in the United States and Europe among individuals smoking flavored-hookah tobacco in order to strengthen the evidence base and to inform the regulation of water pipe products and use.

Rezk-Hanna, & Benowitz, N. L. (2019). Cardiovascular Effects of Hookah Smoking: Potential Implications for Cardiovascular Risk. Nicotine & Tobacco Research, 21(9), 1151–1161. https://doi.org/10.1093/ntr/nty065

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Cardiovascular Effects of Chocolate and Wine - Narrative Review

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Cardiovascular Effects of Chocolate and Wine - Narrative Review

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Posted by Mitchell Watts

I thought this narrative review was interesting and relevant for myself, as it discusses two foods that I enjoy (in moderation): dark chocolate and red wine.

The authors discuss that inflammation and oxidative stress are two important factors that influence the development of atherosclerosis and cardiovascular disease (CVD). Therefore, they focused on the role of the phenolic compounds in red wine and chocolate and its effects on CVD. These polyphenols have anti-inflammatory, antioxidant, and antiplatelet properties that are theoretically beneficial in CVD prevention and treatment.

The authors referenced several different clinical trials, but overall they found that the data suggests a beneficial dose of dark chocolate of 30 to 50 grams per day and for wine 130 to 250 mL per day. For reference, a standard Hershey’s chocolate bar is 43 grams. For wine, a standard serving is 5 ounces (150 mL). Though the authors mentioned cardiovascular risk reduction peaked at 6 to 8 grams of alcohol per day. A standard serving of wine with 12% alcohol would have 14 grams. So risk reduction would potentially peak at half a serving of wine.

Clinically, this review supports the consumption of chocolate and red wine. The antioxidant content of these functional foods may be helpful in the prevention and treatment of atherosclerosis and other cardiovascular diseases. I think this also ties into the benefits of the Mediterranean diet; wine polyphenols may have a synergistic effect with the nutrients and compounds in this dietary pattern.

Though, it is important to note that patients using medications for CVD should be aware of the risk of certain drug-nutrient interactions. I think it’s also important to note about the saturated fat content of chocolate and how this may counteract the benefits of its polyphenols. Though this is potentially debatable with recent research.

Sperkowska, B., Murawska, J., Przybylska, A., Gackowski, M., Kruszewski, S., Durmowicz, M., & Rutkowska, D. (2021). Cardiovascular Effects of Chocolate and Wine-Narrative Review. Nutrients, 13(12), 4269.

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Affiliations

¹ Department of Toxicology and Bromatology, Faculty of Pharmacy, L. Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, A. Jurasza 2 Street, PL-85089 Bydgoszcz, Poland.

² Biophysics Department, Faculty of Pharmacy, L. Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Jagiellońska 13 Street, PL-85067 Bydgoszcz, Poland.

³ Department of Physiotherapy, Faculty of Health Sciences, L. Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Techników 3 Street, PL-85094 Bydgoszcz, Poland.

⁴ Laboratory for Medical Education, Faculty of Medicine, L. Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, St. Florian's 12 Street, PL-85030 Bydgoszcz, Poland.

Free PMC article

Free PMC article

Affiliations

¹ Department of Toxicology and Bromatology, Faculty of Pharmacy, L. Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, A. Jurasza 2 Street, PL-85089 Bydgoszcz, Poland.

² Biophysics Department, Faculty of Pharmacy, L. Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Jagiellońska 13 Street, PL-85067 Bydgoszcz, Poland.

³ Department of Physiotherapy, Faculty of Health Sciences, L. Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Techników 3 Street, PL-85094 Bydgoszcz, Poland.

⁴ Laboratory for Medical Education, Faculty of Medicine, L. Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, St. Florian's 12 Street, PL-85030 Bydgoszcz, Poland.

Abstract

The consumption of food for pleasure is mainly associated with adverse health effects. This review was carried out to verify recent reports on the impact of chocolate and wine consumption on cardiovascular health, with a particular focus on atherosclerosis. On one side, these products have proven adverse effects on the cardiovascular system, but on the other hand, if consumed in optimal amounts, they have cardiovascular benefits. The submitted data suggest that the beneficial doses are 30-50 g and 130/250 mL for chocolate and wine, respectively, for women and men. The accumulated evidence indicates that the active ingredients in the products under consideration in this review are phenolic compounds, characterized by anti-inflammatory, antioxidant, and antiplatelet properties. However, there are also some reports of cardioprotective properties of other compounds such as esters, amines, biogenic amines, amino acids, fatty acids, mineral ingredients, and vitamins. Our narrative review has shown that in meta-analyses of intervention studies, consumption of chocolate and wine was positively associated with the beneficial outcomes associated with the cardiovascular system. In contrast, the assessment with the GRADE (Grading of Recommendations Assessment, Development and Evaluation) scale did not confirm this phenomenon. In addition, mechanisms of action of bioactive compounds present in chocolate and wine depend on some factors, such as age, sex, body weight, and the presence of additional medical conditions. Patients using cardiovascular drugs simultaneously with both products should be alert to the risk of pharmacologically relevant interactions during their use. Our narrative review leads to the conclusion that there is abundant evidence to prove the beneficial impact of consuming both products on cardiovascular health, however some evidence still remains controversial. Many authors of studies included in this review postulated that well-designed, longitudinal studies should be performed to determine the effects of these products and their components on atherosclerosis and other CVD (Cardiovascular Disease) disease.

Keywords: atherosclerosis; bioactive compounds; cardiovascular benefits; cardiovascular risk; chocolate; drug-food interactions; inflammation; oxidative stress; wine.

Conflict of interest statement

The authors declare no conflict of interest.

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Zhang Y., Koradia A., Kamato D., Popat A., Little P.J., Ta H.T. Treatment of atherosclerotic plaque: Perspectives on theranostics. J. Pharm. Pharmacol. 2019;71:1029-1043. doi: 10.1111/jphp.13092. - DOI - PubMed

Teissedre P.L., Stockley C., Boban M., Gambert P., Alba M.O., Flesh M., Ruf J.C. The effects of wine consumption on cardiovascular disease and associated risk factors: A narrative review. Oeno One. 2018;50:67-79. doi: 10.20870/oeno-one.2018.52.1.2129. - DOI

Bittner V. The New 2019 AHA/ACC Guideline on the Primary Prevention of Cardiovascular Disease. Circulation. 2020:2402-2404. doi: 10.1161/CIRCULATIONAHA.119.040625. - DOI - PubMed

Yokose C., McCormick N., Rai S.K., Lu N., Curhan G., Schwarzfuchs D., Shai I., Choi H.K. Effects of low-fat, mediterranean, or low-carbohydrate weight loss diets on serum urate and cardiometabolic risk factors: A secondary analysis of the dietary intervention randomized controlled trial (direct) Diabetes Care. 2020;43:2812-2820. doi: 10.2337/dc20-1002. - DOI - PMC - PubMed

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cardiovascular diseases / prevention & control*

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national center for biotechnology information

# data[].attributes.attachment_link.title
Cardiovascular Effects of Chocolate and Wine-Narrative Review - PubMed

# data[].attributes.attachment_link.description
The consumption of food for pleasure is mainly associated with adverse health effects. This review was carried out to verify recent reports on the impact of chocolate and wine consumption on cardiovascular health, with a particular focus on atherosclerosis. On one side, these products have proven ad ...

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Seonwook Kim: A plant-based diet, atherogenesis, and coronary artery disease prevention

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Seonwook Kim: A plant-based diet, atherogenesis, and coronary artery disease prevention

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Atherosclerosis cannot be reversible after progression, so preventive care is the best way to survive from atherosclerosis. Atherosclerosis is associated with a high dietary intake of meat, fat, and carbohydrates. This condition induces progressive damage to the endothelial cells lining the vascular system, including the heart, leading to endothelial dysfunction
In this study, they investigated the protective effects of a plant-based diet against atherosclerotic coronary artery disease by increasing endothelial protective factors in the circulation while reducing factors that are injurious to endothelial cells. The primary aim of the plant-based diet is to maximize consumption of nutrient-dense plant foods while minimizing processed foods, added sugars, oils, and animal-based foods.
One key finding from this study is that polyphenols derived from dietary plant intake have protective effects on vascular endothelial cells, possibly as antioxidants that prevent the oxidation of low-density lipoprotein. In clinical application, for prevention, people may reduce the consumption of meat, fat, and carbohydrates and consume more dietary plant which contains polyphenol such as fruits, vegetables, and seeds.

Tuso P, Stoll SR, Li WW. A plant-based diet, atherogenesis, and coronary artery disease prevention. Perm J. 2015 Winter;19(1):62-7. doi: 10.7812/TPP/14-036. Epub 2014 Nov 24. PMID: 25431999; PMCID: PMC4315380.

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Affiliations

¹ Physician Leader for Total Health in Southern California. phillip.j.tuso@kp.org.

² Physician for Coordinated Health in Bethlehem, PA. Stollx7@gmail.com.

³ President and Medical Director of the Angiogenesis Foundation of the Institute for Advance Studies in Cambridge, MA. wli@angio.org.

Free PMC article

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Affiliations

¹ Physician Leader for Total Health in Southern California. phillip.j.tuso@kp.org.

² Physician for Coordinated Health in Bethlehem, PA. Stollx7@gmail.com.

³ President and Medical Director of the Angiogenesis Foundation of the Institute for Advance Studies in Cambridge, MA. wli@angio.org.

Abstract

A plant-based diet is increasingly becoming recognized as a healthier alternative to a diet laden with meat. Atherosclerosis associated with high dietary intake of meat, fat, and carbohydrates remains the leading cause of mortality in the US. This condition results from progressive damage to the endothelial cells lining the vascular system, including the heart, leading to endothelial dysfunction. In addition to genetic factors associated with endothelial dysfunction, many dietary and other lifestyle factors, such as tobacco use, high meat and fat intake, and oxidative stress, are implicated in atherogenesis. Polyphenols derived from dietary plant intake have protective effects on vascular endothelial cells, possibly as antioxidants that prevent the oxidation of low-density lipoprotein. Recently, metabolites of L-carnitine, such as trimethylamine-N-oxide, that result from ingestion of red meat have been identified as a potential predictive marker of coronary artery disease (CAD). Metabolism of L-carnitine by the intestinal microbiome is associated with atherosclerosis in omnivores but not in vegetarians, supporting CAD benefits of a plant-based diet. Trimethylamine-N-oxide may cause atherosclerosis via macrophage activation. We suggest that a shift toward a plant-based diet may confer protective effects against atherosclerotic CAD by increasing endothelial protective factors in the circulation while reducing factors that are injurious to endothelial cells. The relative ratio of protective factors to injurious endothelial exposure may be a novel approach to assessing an objective dietary benefit from a plant-based diet. This review provides a mechanistic perspective of the evidence for protection by a plant-based diet against atherosclerotic CAD.

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Critselis, E., Kontogianni, M., Georgousopoulou, E., Chrysohoou, C., Tousoulis, D., Pitsavos, C., & Panagiotakos, D. (2021). Comparison of the Mediterranean diet and the Dietary Approach Stop Hypertension in reducing the risk of 10-year fatal and non-fatal CVD events in healthy adults: The ATTICA Study (2002–2012). Public Health Nutrition, 24(9), 2746-2757. doi:10.1017/S136898002000230X

This study is important because sometimes there is conflicting information and it is hard to know which diet you should go with to have the best outcomes. As CVD development/progression is a complex process of many variables and is such a prevalent disease outcome for the aging population, having a diet that is optimal for preventing CVD is important. This study compared efficacy of the Med diet and the DASH diet in a study cohort of 3042 initial individuals in Athens, Greece that were followed for 10 years with a total of 2020 participants making it through to the end of 10 year follow up.

A key finding is that “high adherence to the Med diet, and not the DASH diet, was associated with a reduction in the frequency and time to occurrence of 10 year fatal and non-fatal CVD.” (p. 2752) People that had high adherence to the DASH diet as compared to low adherence to the DASH diet had similar rates of 10 year CVD manifestation. People with high adherence to the Med diet compared to low adherence had a 4 fold-lower risk of developing CVD even after they adjusted for confounding factors like age, gender, physical activity, weight, smoking, hypertension, etc. Important to note that DASH focuses on lowering hypertension, which is not the only cause of CVD.

The clinical importance of this is that it would be more beneficial to advocate for high adherence to Med diet in Mediterranean populations as well as to try to encourage non-Mediterranean populations to adopt it. One interesting thing that they mentioned is that the Med-diet, in contrast to the westernized DASH diet, has an emphasis that went beyond nutrient intake and encompassed lifestyle practices like physical activity and active social networks which help psychosocial and cognitive function. So even if the food groups of the Med diet are not within your patients palate range, it could be beneficial to encourage social interaction, leisure activities and better sleep quality like the Med diet does in addition to whichever diet your patient is most likely/able to comply with.

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Vitamin B6: A Challenging Link Between Nutrition and Inflammation in CVD- Lydia Duncan

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Vitamin B6: A Challenging Link Between Nutrition and Inflammation in CVD- Lydia Duncan

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For this weeks article, I selected this review of the research on B6 vitamins and their role in Cardiovascular Diseases (CVD). The main purpose of this review was to evaluate the relationship between low vitamin B6 and its link through inflammation to CVD. Vitamin B6 is involved in a number of physiological reactions (ex: regulating cellular metabolism). Leading into my next point (i.e. why it is important), since vitamin B6 is so physiologically important, it makes sense as to why researchers would want to evaluate links between the vitamin and chronic diseases (like CVD). This study is also important because of it's relation of inflammation to CVD. Throughout the semester so far, we have discussed numerous chronic diseases involving inflammation (ex: Diabetes, Arthritis, Ulcerative Colitis, etc.), so I was not surprised to find that inflammation often also plays a role in CVD.

One key finding of this study was that multiple studies showed an association between more mild vitamin B6 deficiencies and inflammation-related diseases, such as CVD. There were also a few studies that showed no association between these two factors though, so more research is needed to fully understand the interactions between vitamin B6 and inflammation, and how they relate to diseases like CVD. Another key finding of this study is that appropriate timing and dosage of B6 vitamins could be a factor in how effective the supplementation is. The article suggests more research on specific timings and dosages of vitamin B6. This is to evaluate if they play a role in why vitamin B6 showed association with inflammation and CVD in some studies, while no association in others. This relates to nutritional sciences because vitamin B6 supplementation is less discussed compared to other vitamin deficiencies. This is interesting to me, especially since it plays such a large role in our metabolism.

One clinical implication of this study is that B6 vitamin status should be evaluated, especially if the patient is at a higher risk for CVD. One recommendation from the article for this was supplementation. But (like the article also states), more studies on vitamin B6 supplementation are needed, so this would be interesting research to continue! Vitamin B6 can be derived from food sources as well though. Some of these include fish, organ meats, starchy vegetables, and non-citrus fruits (2021). Overall, from this study we can see that there is possibly a link between vitamin B6 and inflammation on CVD, but more research is needed to fully justify the association.

Article Citation:
Lotto, V., Choi, S., & Friso, S. (2011). Vitamin B6: A challenging link between nutrition and inflammation in CVD. British Journal of Nutrition, 106(2), 183-195. doi:10.1017/S0007114511000407
Additional Resources:
NIH-ODS. (2021, March 26). Office of dietary supplements - vitamin B6. NIH Office of Dietary Supplements. Retrieved March 22, 2022, from https://ods.od.nih.gov/factsheets/VitaminB6-HealthProfessional/

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The two major derivates of vitamin B ₆ are the coenzyme species pyridoxamine 5′-phosphate and pyridoxal 5′-phosphate (PLP)⁽Reference Shane and Stipanuk ¹⁾. PLP is both the major coenzyme form of vitamin B ₆ in plasma and the metabolically active coenzyme produced by the phosphorylation of the pyridoxal compound following the oxidation of other vitamin B ₆ vitamers in the liver. Plasma PLP is considered as the most sensitive indicator for tissue vitamin B ₆ status because it reflects liver PLP concentrations and stores⁽Reference Stickel, Choi and Kim ²⁻Reference Lumeng, Lui and Li ⁶⁾, while other measures of vitamin B ₆ such as erythrocyte PLP, total plasma B ₆ and urinary excretion of 4-pyridoxic acid are also useful markers of human vitamin B ₆ status but are less commonly available in clinical practice⁽, ⁾. Overt vitamin B ₆ deficiency is a rare condition and is mainly defined by the appearance of specific clinical signs or symptoms, nonetheless a suboptimal vitamin B ₆ status may influence the risk of development of several diseases. It has been previously suggested that vitamin B ₆ deficiency corresponds to plasma PLP concentrations below 20 nmol/l, while a borderline, marginal impairment of vitamin B ₆ status may be observed for plasma PLP levels below 30 nmol/l⁽, ⁾. However, there is no definite consensus for a value that unquestionably defines a deficient state of this nutrient. Vitamin B ₆ deficiency is rather a notion in evolution since novel at-risk pathological conditions seem, due to a grade of impairment that fails, to meet the magnitude of deficit classically defined as a clear vitamin B ₆-deficient status⁽, ⁾.

Several reports have indicated a role of low plasma PLP concentrations in a number of pathological conditions. This suggests that not only does overt vitamin B ₆ deficiency increase the risk of certain chronic diseases, but even mild vitamin B ₆ deficiency could be associated with an increased risk of certain chronic diseases⁽Reference Pasceri and Yeh ¹⁰⁻Reference Fairfield and Fletcher ¹²⁾.

Low plasma PLP concentrations have been reported to be inversely related to C-reactive protein (CRP), a major marker of inflammation and a risk factor for atherosclerotic disease⁽Reference Friso, Jacques and Wilson ¹³, Reference Willerson and Ridker ¹⁴⁾. A number of studies have shown that low plasma vitamin B ₆ levels are associated with typical inflammatory chronic diseases, such as rheumatoid arthritis (RA)⁽Reference Chiang, Bagley and Roubenoff ¹⁵⁾ and inflammatory bowel diseases⁽Reference Saibeni, Cattaneo and Vecchi ¹⁶⁾, and are inversely related to the markers of inflammation⁽Reference Roubenoff, Roubenoff and Selhub ¹⁷, Reference Chiang, Smith and Selhub ¹⁸⁾. These studies suggest that impaired vitamin B ₆ status in RA patients is not solely caused by either lower intake, malabsorption or excessive catabolism of the vitamin, but is rather the result of metabolic mechanisms caused by the inflammatory process⁽Reference Chiang, Smith and Selhub ¹⁸, Reference Chiang, Bagley and Selhub ¹⁹⁾. Among other possible hypotheses, it has also been suggested that the underlying inflammatory condition itself may reduce circulating and hepatic concentrations of PLP by mobilising PLP from the liver and peripheral tissues to the sites of inflammation⁽Reference Chiang, Smith and Selhub ¹⁸, Reference Chiang, Bagley and Selhub ¹⁹⁾. Chiang et al. ⁽Reference Chiang, Smith and Selhub ¹⁸⁾ observed that plasma PLP concentrations in rats with adjuvant arthritis were about 53 % of the controls at acme of inflammation and related to the content of PLP in the liver, thus suggesting that the lower circulating PLP levels observed in RA could be a sign of a decrease in hepatic PLP pools, and that plasma PLP is a valuable indicator of liver vitamin B ₆ status during inflammation. Further data showed that PLP in plasma seems a more relevant metabolic marker than PLP in the erythrocytes during inflammation⁽Reference Chiang, Bagley and Selhub ¹⁹⁾ as also confirmed by the observation that plasma, but not erythrocyte PLP concentrations, inversely relates to both clinical and biochemical indices of disease activity and severity in patients affected by RA⁽Reference Chiang, Bagley and Selhub ¹⁹⁾.

For decades, several studies have demonstrated that patients with RA or other inflammatory diseases have a higher risk of developing premature coronary artery disease (CAD)⁽Reference Monson and Hall ²⁰, Reference Mikuls and Saag ²¹⁾ and traditional CVD risk factors did not, by themselves, clarify the increased prevalence of CAD in such patients⁽Reference del Rincon, Williams and Stern ²²⁾. Through studying the relationship between RA, inflammation and CAD, some CVD prevention strategies in RA patients have been proposed, including anti-inflammatory therapy with cyclo-oxygenase-2-specific inhibitors and statins⁽Reference Snow and Mikuls ²³⁾ as well as pyridoxine hydrochloride supplementation⁽Reference Chiang, Selhub and Bagley ²⁴⁾. Several studies, moreover, have confirmed the theory of atherosclerosis as an inflammatory disease, thus demonstrating that the link between atherosclerosis, RA and other inflammatory chronic diseases is through inflammatory processes. Inflammation may therefore be considered as a major pathogenic mediator underlying atherosclerosis and its complications⁽, Reference Libby, Ridker and Hansson ²⁶⁾. The chronic inflammation in atherosclerotic-related disease, such as CAD and stroke, and its major clinical complications, namely myocardial infarction (MI), have also been associated with low plasma vitamin B ₆ concentrations⁽Reference Friso, Girelli and Martinelli ¹¹, Reference Robinson, Mayer and Miller ²⁷⁻Reference Kelly, Shih and Kistler ²⁹⁾.

The relationship between atherosclerosis and vitamin B ₆-linked inflammatory mechanisms is indeed of great interest. Does low plasma PLP indicate the sole effect of inflammation? Or could it be a cofactor that promotes the development of inflammation, potentially contributing to a sustained chronic inflammatory response? The answer to these questions may open a way to novel and interesting approaches for dietary prevention and therapy.

Vitamin B₆ and coronary artery disease, myocardial infarction and ischaemic stroke

Vitamin B₆ supplementation, inflammation and CVD prevention

An early observation of patients given vitamin B ₆ for inflammatory diseases or degenerative diseases found that subjects supplemented with vitamin B ₆ had a lower risk of developing MI compared with patients who had not taken vitamin B ₆⁽Reference Ellis and McCully ⁵⁵⁾. Table 3 summarises the main studies in which B vitamin supplementation, including supplementation with vitamin B ₆, has been performed. In the Nurses' Health Study, among women with no prior history of CAD, users of multivitamins containing folate and vitamin B ₆ had a reduced risk of CAD⁽Reference Rimm, Willett and Hu ⁵⁶⁾.

Very few human studies have been performed to evaluate the modifications of major markers of inflammation during supplementation with B vitamins, including vitamin B ₆, despite the association with either folate and/or vitamin B ₁₂⁽Reference Peeters, van Aken and Blom ⁵⁷, ⁾. Furthermore, results from these studies have shown that CRP and pro-inflammatory IL levels are unchanged after vitamin supplementation⁽Reference Peeters, van Aken and Blom ⁵⁷, ⁾. Antioxidant activity of vitamin B ₆ supplementation has been observed in a study performed on rats, but the exact mechanism is unclear⁽Reference Mahfouz and Kummerow ⁵⁹⁾.

Several large, prospective trials have been conducted in recent years with the principal aim of studying the effects of lowering serum homocysteine concentrations with the use of B vitamins, including vitamin B ₆, on cardiovascular events⁽Reference Toole, Sane and Bettermann ⁶⁰, Reference Bønaa, Njolstad and Ueland ⁶¹⁾.

Overall, the most compelling data from vitamin supplementation studies have demonstrated that vitamin B ₆ is not effective for preventing the recurrence of cardiovascular events, including CAD, peripheral vascular disease and stroke⁽Reference Wilmink, Welch and Quick ⁵⁴, Reference Albert, Cook and Gaziano ⁶², Reference Toole, Malinow and Chambless ⁶³⁾.

Only a few small trials, performed with renal transplant patients that have hyperhomocysteinaemia and subjects at risk for cerebral ischaemia, have demonstrated the effectiveness of vitamin B ₆ supplementation with folate and vitamin B ₁₂ on carotid artery intima-media thickness progression⁽Reference Marcucci, Zanazzi and Bertoni ⁶⁴, Reference Till, Rohl and Jentsch ⁶⁵⁾. This marker for subclinical atherosclerosis was also evaluated in another recent double-blind, placebo-controlled, randomised clinical trial⁽Reference Hodis, Mack and Dustin ⁶⁶⁾. Vitamin supplementation significantly reduced subclinical atherosclerosis progression only in subjects at low risk for CVD, with total plasma homocysteine concentrations equal to or above 9·1 μmol/l⁽Reference Hodis, Mack and Dustin ⁶⁶⁾. Other trials evaluated CAD patients for the effects of B vitamin supplementation, though the interpretation of the results was ambiguous. Supplementation with vitamin B ₆, folate and vitamin B ₁₂ after coronary angioplasty decreased the rate of restenosis and the need for revascularisation⁽Reference Schnyder, Roffi and Pin ⁶⁷⁾, while supplementation after coronary stenting increased the risk of in-stent restenosis and the need for target-vessel revascularisation⁽Reference Lange, Suryapranata and De Luca ⁶⁸⁾.

Despite the advantage of large randomised intervention studies, wisdom from the studies of cancer chemoprevention with folate clearly suggests that two critical factors should be taken into account in the aforementioned trials: time and dose of B vitamin supplementation. Nutritional intervention is indeed considered to be a two-edged sword, where a beneficial effect may be observed with nutritional support in the prevention phase and a disease-aggravating effect may be observed after the onset of illness, with nutritional support actually fuelling the disease process. This observation may certainly apply to folate supplementation, which can effectively prevent the onset or progression of disease in the early phase, while it may accelerate the progression of disease in the late phase. It can therefore be speculated that continuous supplementation with a single non-physiological form of vitamin supplements might contribute to unexpected or even harmful outcomes, even in the at-risk condition of having an impaired vitamin B ₆ status. Furthermore, the major endpoints of these studies were those of evaluating the effect of lowering plasma homocysteinaemia on the recurrence of established disease, mainly by the simultaneous use of various B vitamins that have many additional functions other than that of lowering total plasma homocysteine. Little information, however, is available regarding both the effects of vitamin B ₆ supplementation on inflammatory markers and the correct dose and timing to be followed to avoid the possible harmful effect of excessive or inappropriate vitamin B ₆ supplementation. This information that would be needed for a possible primary or secondary preventive approach using vitamin B ₆ is to be developed. Further specific studies are required to deepen our knowledge in this regard.

Even if there is consistently a lack of benefit in secondary prevention of CVD with B vitamin supplementation, with or without vitamin B ₆ (Western Norway B Vitamin Intervention Trial⁽Reference Ebbing, Bleie and Ueland ⁶⁹⁾, Women's Antioxidant and Folic Acid Cardiovascular study⁽Reference Albert, Cook and Gaziano ⁶²⁾, Vitamin Intervention for Stroke Prevention randomised controlled trial⁽Reference Toole, Malinow and Chambless ⁶³⁾, Norwegian Vitamin Trial⁽Reference Bønaa, Njolstad and Ueland ⁶¹⁾, Heart Outcomes Prevention Evaluation 2⁽Reference Lonn, Yusuf and Arnold ⁷⁰⁾), it should also be considered that all the aforementioned studies are quite diverse from one another in terms of the time period of supplementation. In fact, one may raise the point that the time period of supplementation is especially critical to reach positive outcomes or avoid possible harmful effects in terms of the rate of CVD events⁽⁾. However, despite the apparently clear outcomes⁽⁾, it could be argued that a potential benefit that modifies secondary prevention outcomes may not be observed over a period of moderate duration (between 2 and 5 years for the Norwegian Vitamin Trial, Heart Outcomes Prevention Evaluation 2 and Vitamin Intervention for Stroke Prevention studies or of about 7 years for the Women's Antioxidant and Folic Acid Cardiovascular study).

Furthermore, the negative results of vitamin supplementation trials, including vitamin B ₆ use, do not preclude the possibility of a protective effect in primary prevention. It could be difficult, however, to demonstrate that vitamin B supplementation is ineffective in patients who have had a clinical vascular event, while effective in those without a clinical event or with subclinical atherosclerosis. Clinical trials for primary prevention may require a longer duration and larger populations in order to answer the key question on whether vitamin B ₆ supplementation is effective in preventing CAD before the first vascular event or in younger life.

Studies are needed to find the specific time and optimal dose of vitamin B ₆ in order to maximise efficacy, minimise adverse effects and identify targets for vitamin B ₆ interventions on the basis of genetic susceptibility and environmental factors. A better understanding of the mechanisms underlying the relationship between CVD and vitamin B ₆ may indeed be extremely helpful in designing the most accurate preventive strategies.

Inflammation and vitamin B₆-related atherogenesis

PLP functions as a coenzyme in more than 100 reactions that are involved in the metabolic pathways of neurotransmitters as well as in the metabolism of amino acids, lipids and carbohydrates⁽Reference Endo, Nishiyama and Otsuka ⁷²⁾. PLP also takes part in other significant pathways related to immune function⁽Reference Meydani, Hayek and Coleman ⁷³⁾, thrombosis⁽, Reference Schoene, Chanmugam and Reynolds ⁷⁵⁾ and inflammation⁽Reference Roubenoff, Roubenoff and Selhub ¹⁷⁾, all of which are crucial mechanisms in every stage of the atherosclerotic process.

Furthermore, PLP is implicated in the synthesis and repair of both nucleic acids and proteins. Low vitamin B ₆ concentrations could thus reflect an increased consumption of PLP in the accelerated synthesis of cytokines⁽Reference Doke, Inagaki and Hayakawa ⁷⁶⁾ and in the activation and proliferation of lymphocytes, both of which are key events in the inflammatory process⁽Reference Meydani, Ribaya-Mercado and Russell ⁷⁷, Reference Kwak, Hansen and Leklem ⁷⁸⁾.

Considering the epidemiological evidence of a role of vitamin B ₆ in inflammatory-related diseases and the observed relationship with inflammatory markers⁽Reference Friso, Girelli and Martinelli ¹¹, Reference Saibeni, Cattaneo and Vecchi ¹⁶, Reference Chiang, Smith and Selhub ¹⁸, Reference Morris, Sakakeeny and Jacques ⁷⁹⁾, it is plausible that vitamin B ₆ plays a role in CVD pathogenesis through mechanisms linked to inflammation ( Table 4).

Therefore, with the knowledge that systemic acute-phase markers are solid and independent risk factors for CAD⁽, Reference Ridker, Hennekens and Buring ⁸¹⁾, that inflammation exerts an essential role in all stages of the atherosclerotic process⁽⁾ and the possibility that vitamin B ₆ has a role in inflammatory processes, several mechanisms were proposed linking low vitamin B ₆ and CVD using cell culture studies, animal studies⁽Reference Endo, Nishiyama and Otsuka ⁷²⁾ and clinical trials.

Animal studies have reported that inflammation reduces circulating and hepatic concentrations of vitamin B ₆. Plasma PLP is considered as a sensitive indicator of tissue vitamin B ₆ status⁽Reference Parker, Marshall and Roberts ³⁻, Reference Chiang, Bagley and Roubenoff ¹⁵, Reference Chiang, Smith and Selhub ¹⁸⁾. As shown in Fig. 1, it is thus possible that, in patients in an inflammatory state, PLP is mobilised from the liver and peripheral tissues to the sites of inflammation⁽Reference Chiang, Bagley and Selhub ¹⁹⁾. Plasma PLP levels are known to be inversely related to TNF-α production and other inflammatory cytokines in RA⁽Reference Roubenoff, Roubenoff and Selhub ¹⁷⁾. It has also been reported that low plasma PLP concentrations are inversely related to both plasma fibrinogen⁽Reference James, Vorster and Venter ⁸³⁾ and CRP⁽Reference Friso, Girelli and Martinelli ¹¹, Reference Friso, Jacques and Wilson ¹³⁾, with a robust and independent association of other major biomarkers related to vitamin B ₆ metabolism⁽Reference Friso, Girelli and Martinelli ¹¹⁾. Moreover, inflammatory status increases oxidant stress, which results from an imbalance between oxidant production and antioxidant defences ( Fig. 1). All these conditions characterised by the increase in inflammatory cytokines, fibrinogen, CRP and superoxide radicals may induce the consumption of vitamin B ₆, with a consequent reduction of PLP plasma levels and its antioxidant effect, and, at the same time, they may favour a thrombogenic effect, thus triggering an impairment of endothelial function which is a key event in the pathogenesis of atherosclerotic processes ( Fig. 1)⁽Reference Heitzer, Schlinzig and Krohn ⁸⁴⁾. PLP has also been described to have an inhibitory effect on endothelial cell proliferation⁽Reference Matsubara, Matsumoto and Mizushina ⁸⁵, Reference Matsubara, Mori and Akagi ⁸⁶⁾. The persistence of a chronic inflammatory condition may result in the depletion of vitamin B ₆, which might then contribute to a sustained chronic inflammatory response ( Fig. 1).

Most of the evidence demonstrates a potential role for vitamin B ₆ in inflammatory processes where the low vitamin B ₆ status in inflammation-related illnesses appears to result not from lower intake or excessive catabolism of PLP but from the inflammatory process underlying the disease itself⁽Reference Morris, Sakakeeny and Jacques ⁷⁹⁾.

Although vitamin B ₆ represents an important coenzyme in the metabolism of homocysteine, a recognised risk factor for thrombosis, the role of PLP in atherosclerosis is only partly related to its function in the one-carbon pathway. Several studies have thus supported a role for vitamin B ₆ in the risk of CVD⁽Reference Robinson, Mayer and Miller ²⁷, Reference Folsom, Nieto and McGovern ³¹, Reference Chasan-Taber, Selhub and Rosenberg ⁴², Reference Verhoef, Stampfer and Buring ⁴⁶⁾ and stroke⁽Reference Kelly, Shih and Kistler ²⁹⁾, independent of homocysteine and other risk factors. A hypothesis is that vitamin B ₆ could be directly implicated as a cofactor in an anti-inflammatory mechanism where the utilisation of the vitamin results in its consumption, and the consequent low vitamin B ₆ concentrations could support and amplify the inflammatory process, thereby leading to chronic progression of inflammatory disease. Indeed, a mild deficiency of vitamin B ₆ may be associated with an increased risk, not only of atherosclerosis, but also of other chronic inflammatory diseases such as RA⁽Reference Chiang, Smith and Selhub ¹⁸, Reference Woolf and Manore ⁸⁷⁾ and inflammatory bowel diseases⁽Reference Saibeni, Cattaneo and Vecchi ¹⁶⁾. A number of studies have highlighted the relationship between PLP and inflammation, showing an inverse association between vitamin B ₆ and major markers of inflammation, including plasma fibrinogen concentration⁽Reference James, Vorster and Venter ⁸³⁾, erythrocyte sedimentation rate and CRP⁽Reference Friso, Jacques and Wilson ¹³⁾. In the population-based Framingham Heart Study cohort, the association between PLP and CRP was strong and independent of other major biomarkers related to vitamin B ₆ metabolism⁽Reference Friso, Jacques and Wilson ¹³⁾, supporting a possible role for plasma PLP in inflammatory processes.

Some reports did not support this observation⁽Reference Folsom, Desvarieux and Nieto ⁸⁸⁾, such as the study by Folsom et al. ⁽Reference Folsom, Desvarieux and Nieto ⁸⁸⁾, conducted among healthy middle-aged adults in the Atherosclerosis Risk in Communities Study, which did not find an inverse association between CRP and PLP. However, the authors did observe that lower plasma PLP and dietary vitamin B ₆ were associated with a higher leucocyte count, though this association was not found with the use of vitamin supplements⁽Reference Folsom, Desvarieux and Nieto ⁸⁸⁾. It should also be taken into account that some diversity in the observations reported by the studies may be due to the different methods utilised to measure plasma PLP, although the methods used by most studies are considered highly reliable for the assessment of vitamin B ₆ status⁽Reference Friso, Girelli and Martinelli ¹¹, Reference Chiang, Bagley and Roubenoff ¹⁵, Reference Folsom, Desvarieux and Nieto ⁸⁸⁻Reference Kimura, Kanehira and Yokoi ⁹⁰⁾. The majority of studies, however, confirmed the inverse correlation between PLP and major markers of inflammation in various inflammation-related diseases. In subjects affected by RA⁽Reference Chiang, Bagley and Selhub ¹⁹, Reference Chiang, Selhub and Bagley ²⁴⁾, PLP was associated with erythrocyte sedimentation rate, CRP levels and other markers of disease activity and severity, suggesting that impaired vitamin B ₆ status is a result of inflammation. It also appeared that the relationship between lower vitamin B ₆ and increased inflammation in these RA patients could be tissue-specific⁽Reference Chiang, Selhub and Bagley ²⁴⁾.

Plasma PLP concentrations are also altered in subjects who have acute diseases with an evident underlying inflammatory condition. Vasilaki et al. ⁽Reference Vasilaki, McMillan and Kinsella ⁹¹⁾ observed that in patients admitted to an intensive therapy unit, high concentrations of CRP, PLP and intracellular pyridoxal levels were significantly lower in those critically ill patients than in the group of subjects taken as controls.

Further support for the hypothesis of a link between vitamin B ₆ and inflammation can be found in an analysis of data from a large population-based survey from participants in the 2003-4 National Health and Nutrition Examination Survey. Results showed that higher vitamin B ₆ intakes are protective against inflammation, as indicated by hs-CRP concentrations. Moreover, the level of vitamin B ₆ intake that was associated with maximum protection against vitamin B ₆ inadequacy was elevated in the presence of inflammation compared with its absence⁽Reference Morris, Sakakeeny and Jacques ⁷⁹⁾.

A strong inverse association between vitamin B ₆ status, as measured by plasma PLP concentration, and the inflammatory marker CRP was also observed recently in a cohort of elderly Puerto Ricans living in Massachusetts⁽Reference Shen, Lai and Mattei ⁹²⁾. In the present study, chronic inflammatory conditions, such as the metabolic syndrome, diabetes and obesity, were significantly associated with lower plasma PLP. The patients affected by such diseases were also significantly more likely to demonstrate vitamin B ₆ inadequacy. Furthermore, lower PLP plasma concentrations were associated with oxidative stress, as indicated by higher urinary concentrations of 8-hydroxydeoxyguanosine, a marker of DNA damage and oxidative stress⁽Reference Shen, Lai and Mattei ⁹²⁾. Authors concluded that vitamin B ₆ status may influence CAD risk through mechanisms that link vitamin B ₆ to inflammatory processes rather than mechanisms related to the role of vitamin B ₆ in homocysteine metabolism⁽Reference Shen, Lai and Mattei ⁹²⁾.

Conclusions

Several studies have demonstrated an association between mild vitamin B ₆ deficiency with inflammation-related diseases, including CVD⁽Reference Friso, Girelli and Martinelli ¹¹, Reference Saibeni, Cattaneo and Vecchi ¹⁶, Reference Chiang, Smith and Selhub ¹⁸, Reference Morris, Sakakeeny and Jacques ⁷⁹⁾, by highlighting an inverse relationship between vitamin B ₆ and inflammatory markers⁽Reference Friso, Girelli and Martinelli ¹¹, Reference Chiang, Bagley and Selhub ¹⁹, Reference Morris, Sakakeeny and Jacques ⁷⁹⁾. In a consistent number of studies, this association between impaired vitamin B ₆ status and higher risk of CVD is independent of other major traditional atherosclerosis risk factors⁽Reference Friso, Jacques and Wilson ¹³, Reference Robinson, Mayer and Miller ²⁷, Reference Cheng, Lin and Liaw ³⁷, Reference Verhoef, Stampfer and Buring ⁴⁶, Reference Page, Ma and Chiuve ⁴⁴⁾ and is inversely related to the major markers of inflammation⁽Reference Friso, Girelli and Martinelli ¹¹⁾. This evidence suggests a link between impaired vitamin B ₆ and CVD through inflammation. Because vitamin B ₆ is involved in a large number of physiological reactions, it could be essential to design appropriate studies to define the exact mechanisms underlying the inter-relationships among suboptimal vitamin B ₆ status, as defined by both plasma and tissue PLP concentrations, and biochemical-molecular alterations leading to the development of inflammation-related diseases. A research priority may be that of investigating the kinetics and regulation of B ₆ vitamers and enzymes in different body compartments during inflammatory processes.

Mild vitamin B ₆ deficiency is not a rare occurrence in population-based studies⁽Reference Fairfield and Fletcher ¹²⁾. This issue, therefore, deserves further investigation, especially in terms of prevention strategies, for the purpose of promoting specific public health policies. Current clinical trials have indicated that vitamin B ₆ supplementation seems not to be effective for the prevention of recurrence of CVD, although the appropriate dosage and timing for possible beneficial effects through the use of vitamin supplements still remains to be discussed. Other crucial issues pertain also to the evaluation of the actual effect of supplementation with vitamin B ₆ in synthetic form, as well as to whether such approach may be as effective as an adequate dietary vitamin B ₆ intake. The question of whether supplementation with vitamin B ₆ may be useful for primary prevention of CVD is yet another key issue to be defined. The importance of considering vitamin B ₆ status in relation to the risk for CVD may nevertheless open new insights for the potential identification of innovative preventive and therapeutic strategies. In order to help tailor an adequate nutritional approach on an individual basis, both dose and timing as well as the possible harmful effect of vitamin B ₆ supplementation should be carefully considered in the design of future ad hoc clinical trials that are aimed at identifying appropriate vitamin B ₆ supplementation.

The notion of a definite vitamin B ₆ deficiency is a concept to be considered in fieri since the risk of certain diseases seems to be associated with a degree of vitamin B ₆ impairment that falls short of the classical definition of a clear vitamin B ₆-deficient state.

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Vitamin B6: a challenging link between nutrition and inflammation in CVD | British Journal of Nutrition | Cambridge Core

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The two major derivates of vitamin B 6 are the coenzyme species pyridoxamine 5′-phosphate and pyridoxal 5′-phosphate (PLP)( Reference Shane and Stipanuk 1 ). PLP is both the major coenzyme form of vitamin B 6 in plasma and the metabolically active coenzyme produced by the phosphorylation of the pyridoxal compound following the oxidation of other vitamin B 6 vitamers in the liver.

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Mediterranean diet and endothelial function in patients with coronary heart disease: An analysis of the CORDIOPREV randomized controlled trial- Esraa Zamzami

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Mediterranean diet and endothelial function in patients with coronary heart disease: An analysis of the CORDIOPREV randomized controlled trial- Esraa Zamzami

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For this week, the article I chose talks about the Mediterranean diet and its influence on the cardiovascular system and especially on endothelial function. Endothelial dysfunction is related to higher cardiovascular events, and diet can greatly improve this dysfunction and, eventually, cardiovascular health. In this randomized controlled trial, the researchers studied the effect of a Mediterranean diet or a low-fat diet on endothelial function. They found that the Mediterranean diet increased flow-mediated dilation (FMD), which means increased blood flow due to artery dilation. In addition, an increase in endothelial repair and a decrease in endothelial damage was also observed in the group on the Mediterranean diet. However, no changes were seen in the group consuming the low-fat diet.

According to this trial, the clinical implication of this study is that a Mediterranean diet could be beneficial to CVD patients. Enhancing blood flow is a critical aspect of a healthy cardiovascular system. On the other hand, a low-fat diet does not seem beneficial for CVD patients.

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Mediterranean diet and endothelial function in patients with coronary heart disease: An analysis of the CORDIOPREV randomized controlled trial

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Jose Lopez-Miranda and colleagues compare endothelial function in patients with coronary heart disease who consumed different healthy diets.

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Olive oil intake and risk of cardiovascular disease and mortality in the PREDIMED Study

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Olive oil intake and risk of cardiovascular disease and mortality in the PREDIMED Study

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Emalee Haynes
Olive oil intake and risk of cardiovascular disease and mortality in the PREDIMED Study - PubMed (nih.gov)

This randomized, controlled trial worked to determine if there was a link between the amounts of olive oil consumption and cardiovascular disease. The participants included 7,216 men and women ranging from age 55-80 on either Mediterranean diet with supplements of nuts or extra-virgin olive oil, or on a controlled low-fat diet (2014). With this study they were randomized to follow each diet regimen with the inclusion of olive oil in one group, then were followed up with about 5 years later to determine how many developed cardiovascular diseases, had a cardiac event, or died due to cardiac causes. This study found that consuming “extra-virgin olive oil was linked to reduction of risk of cardiovascular disease and mortality in individuals at high cardiovascular risk.” This is an important aspect to mention for patients with cardiovascular disease or at risk for development and connects to nutrition through the consumption of olive oil and dietary recommendations. The clinical implications of this study are evidence supporting consumption of olive oil with potential benefits for patients at high cardiovascular risk.

Guasch-Ferré, Marta et al. “Olive oil intake and risk of cardiovascular disease and mortality in the PREDIMED Study.” BMC medicine vol. 12 78. 13 May. 2014, doi:10.1186/1741-7015-12-78

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Katelyn Spain: Components of a Cardioprotective Diet New Insights

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Katelyn Spain: Components of a Cardioprotective Diet New Insights

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Dietary factors have been found to have the greatest potential for reducing cardiovascular diseases. The purpose of this study is to review different types of foods to allow people to prioritize foods and dietary habits that are better for reducing cardiovascular diseases. Besides what nutrients are present in foods, people need to know the carbohydrate and fat quantities and qualities of foods, sodium consumption, and how to maintain energy balance. Fruits and vegetables have been found to reduce high blood pressure, lipid levels, and impact weight control. The micronutrients and fibers within fruits and vegetables allow for this. Greater consumption of fruits and vegetables has been found to reduce the risk of CVD. Whole grains are where patients need to focus on the carbohydrate quantities and qualities, the processing of these foods can lead to added sugars and starches. With less processed whole grain foods, there is a reduced risk in endothelial inflammation. Red meat can increase CVD risk and it has been found that lower consumption of red meat improves CVD health risks. It was also found that how different meats are cooked and process can also influence CVD risks. These were some of the foods that this article discussed. Clinical implications of this would be for physicians, nutritionists, and other health care professionals to advise patients struggling with CVD to consider changing their dietary lifestyle. They can help patients by telling them what to avoid and what to add to their diets.
Mozaffarian, D., Appel, L. J., & Van Horn, L. (2011). Components of a cardioprotective diet: new insights. Circulation, 123(24), 2870–2891. https://doi.org/10.1161/CIRCULATIONAHA.110.968735

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Circulation. Author manuscript; available in PMC 2018 Nov 28.

Published in final edited form as:

The global burdens of cardiovascular diseases (CVD), type 2 diabetes mellitus (DM), and obesity are rising, producing enormous losses of life and disability-adjusted life-years in both developed and developing nations.1 Most of these burdens are preventable and are occurring at unnecessarily younger ages, largely owing to suboptimal lifestyle, which includes poor diet quality, excess caloric intake, physical inactivity, and smoking.2-5 Worldwide, striking differences in dietary habits and rates of chronic diseases exist. The identification and targeting of dietary factors with the greatest potential for reducing CVD, DM, and obesity are of major scientific and public health importance.

The science of diet and chronic disease is relatively young, spanning perhaps only half a century.6 New advances offer substantial evidence from complementary research paradigms on cardiometabolic effects of specific dietary factors. Several recent evidence-based reviews conducted in conjunction with national and international policy-making efforts provide the context for the present report. The need to prioritize selected foods and overall dietary patterns rather than only individual nutrients, the relevance of carbohydrate and fat quality as well as quantity, the effects and policy implications of sodium consumption, the importance of energy balance, and the role of dietary supplements represent several key findings of interest. Evidence-based insights into successful individual and public health strategies for behavior change are also addressed. Overall, the present report is intended to provide a useful framework for health practitioners and policy makers to understand contemporary issues related to the effects of diet on CVD.

Methods

Evidence for effects of dietary factors on cardiometabolic health was reviewed, often derived from recent comprehensive reviews performed for policy-making or similar activities, including those of the American Heart Association (AHA) 2020 Impact Goals Committee (D.M., L.J.A.),7 the AHA Nutrition Committee (D.M., L.J.A.,L.V.H.),8,9 the US Dietary Guidelines Advisory Committee (L.J.A.,L.V.H.),10 the World Health Organization Expert Consultation on Fats and Fatty Acids in Human Nutrition (D.M.),11 the World Health Organization Global Burden of Diseases, Risk Factors, and Injuries Nutrition and Chronic Diseases Expert Group (D.M.),12 and the Institute of Medicine Report on Strategies to Reduce Sodium Intake(L.J.A.).13 The views expressed in the present report are those of the authors and do not necessarily represent the views or conclusions of the committees on which they served.

The present report was not intended to cover all possible nutritional topics related to CVD. Rather, it reviews selected topics with reasonably robust evidence yielding important new insights. Several relevant criteria currently used to evaluate evidence for effects of dietary habits on chronic diseases were adopted, including those of Bradford Hill,14 the World Health Organization,15 and similar criteria. Evidence from human studies evaluating established cardio-metabolic risk factors or clinical end points was prioritized, including systematic reviews that provided quantitative pooled effect estimates from multiple studies.

Foods

Randomized, controlled trials (RCTs) of cardiometabolic risk factors and prospective cohort studies of disease end points provide strong concordant evidence for cardiovascular effects of several specific foods. In contrast with individual nutrients in isolation, health effects of foods likely represent the synergy of composite effects and interactions of multiple factors, including carbohydrate quality, fiber content, specific fatty acids and proteins, preparation methods, food structure, and bioavailability of inherent micronutrients and phyto-chemicals. Dietary patterns based on particular foods/components ( Table 1 ) have established cardiometabolic benefits and are higher in dietary fiber, healthy fatty acids, vitamins, antioxidants, potassium, other minerals, and phyto-chemicals and lower in refined carbohydrates, sugars, salt, saturated fatty acid (SFA), dietary cholesterol, and trans fat.

Table 1.

Goal†

Serving Sizes

Nutrient Benefits

Whole grains ‡

3+ servings per day, in place of refined grains

1 slice of whole grain bread; 1 cup of high-fiber whole grain cereal; ½ cup of cooked whole grain rice, pasta, or cereal.

Whole grains contribute B vitamins, vitamin E, fiber, folate, and other nutrients; enhance satiety; and displace consumption of refined carbohydrates. Three servings of whole grains contribute ~210-450 kcal.

Fats, oils, or foods containing or made with partially hydrogenated vegetable oils

Avoid intake

Reduced consumption of industrially produced trans fatty acids.

Alcohol §

For those who consume alcohol, up to 2 daily for men, 1 daily for women

5 oz wine; 12 oz beer; 1.5 oz spirits

Moderate alcohol use raises HDL cholesterol, improves insulin sensitivity, and reduces systemic inflammation.

Energy balance

Reduce portion sizes, increase physical activity (minimum 150 min/wk moderate or 75 min/wk vigorous activity) ∥, limit TV watching, and ensure adequate sleep.

For an average 73-kg adult, 1 hour of brisk walking burns ~277 kcal; hiking, 438 kcal; swimming, 511 kcal; and jogging, tennis, or basketball, 584 kcal.18

Fruits and Vegetables

In RCTs, diets that emphasize consumption of fruits and vegetables produce substantial improvements in several risk factors, including blood pressure (BP), lipid levels, insulin resistance, inflammatory biomarker levels, endothelial function, and weight control.19-25 Benefits do not appear reproducible with equivalent amounts of representative mineral and fiber supplements,26 nor are they dependent on dietary macronutrient (fat, protein, or carbohydrate) composition.22 This evidence suggests that benefits might be derived from (1) a more complex set of micronutrients, phytochemicals, and fiber found in fruits and vegetables; (2) potentially enhanced bioavailability of these nutrients in their natural state; and/or (3) replacement of less healthful foods in the diet. In long-term observational studies, greater fruit and vegetable consumption are each associated with lower incidence of coronary heart disease (CHD), and greater fruit consumption is associated with lower incidence of stroke ( Figure 1 ).27,28 The results of RCTs of physiological measures and prospective cohorts of disease outcomes together provide strong concordant evidence that fruit and vegetable consumption lowers CVD risk ( Table 2 ). Potential differences in health effects contributed by specific types of fruits, vegetables, or their juices require further investigation.

Table 2.

Ecologic Studies of Clinical End Points*

Randomized Trials of Risk Factors†

Prospective Cohort Studies of Clinical End Points*

Randomized Trials of Clinical End Points*

Nutrients ‡

Carbohydrate ∥

+++ ↑

++++ ↑↔ §

++++ ↔

+ ↔

Seafood omega-3 fatty acids

+++ ↓

++++ ↓

++++ ↓ †

++ ↓

Plant omega-3 fatty acids

++ ↓

++ ↓

++ ↓ †

+ ↔

Whole Grains

Although no single accepted definition of whole grain exists, whole grains generally comprise bran, germ, and endosperm from the natural cereal. Bran contains soluble and insoluble dietary fiber, B vitamins, minerals, flavonoids, and tocopherols; germ contains numerous fatty acids, antioxidants, and phytochemicals. Endosperm provides largely starch (carbohydrate polysaccharides) and storage proteins.30 The type and extent of processing appear to modify the health effects of grain and carbohydrate consumption ( Figure 2 ). For example, removal of bran and germ reduces dietary fiber that has important benefits, including lowering of BP and cholesterol levels31,32; increases bioavailability and rapidity of digestion of remaining endosperm, which increases glycemic responses33; and eliminates minerals, micronutrients, and other phytochemicals that may have additional independent health benefits16 (see "Carbohydrate Amount and Quality").

In RCTs, consumption of whole grains improves glucose-insulin homeostasis and endothelial function and possibly reduces inflammation and improves weight loss.34-36 Consumption of whole grain oats reduces low-density lipoprotein (LDL) cholesterol without reducing high-density lipoprotein cholesterol or raising triglycerides.37 Consistent with physiological benefits, greater whole grain consumption is associated with lower incidence of CHD, DM, and possibly stroke ( Figure 1 ). The higher dietary fiber in whole grains contributes to these benefits. In RCTs, increased dietary fiber reduces serum triglycerides, LDL cholesterol, blood glucose, and BP.31,32 Emerging evidence supports additional independent contributions to health from other characteristics of whole grains, including slower digestion (lower glycemic responses) and higher content of minerals, phytochemicals, and fatty acids.16,17 Thus, similar to fruits and vegetables, health effects of whole grains may result from synergistic effects of multiple constituents that are unlikely to be matched by supplemental fiber alone, added bran, or isolated micronutrients, as well as from dietary substitution for more highly refined/processed carbohydrates and starches that may themselves induce adverse cardiometabolic effects (see "Carbohydrate Amount and Quality").

Improved nutritional assessment techniques and databases are needed to further quantify and evaluate potential contributions to health of each component of whole grains. Evidence-based yet pragmatic definitions of what constitutes a whole grain food ( Figure 2 ) are also essential to reduce public confusion and allow consumers to choose healthy grains wisely. As one example, to help monitor national progress toward achieving dietary goals, the AHA 2020 Impact Goals developed a pragmatic definition of whole grains based on the fiber content of whole wheat, ie, ≥1.1 g of naturally occurring dietary fiber per 10 g of carbohydrate in the grain product (eg, bread, cracker, etc).7

Fish

Fish and other seafood contain several healthful constituents, including specific proteins, unsaturated fats, vitamin D, selenium, and long-chain omega-3 polyunsaturated fatty acids (PUFAs), which include eicosapentaenoic acid (EPA; 20:5 omega-3) and docosahexaenoic acid (DHA; 22:6 omega-3). In humans, EPA and especially DHA are synthesized in low amounts (<5%) from their plant-derived precursor, α-linolenic acid (18:3 omega-3).38 Thus, tissue levels of EPA plus DHA are strongly influenced by their direct dietary consumption. Average EPA plus DHA contents of different seafood species vary by >10-fold. Fatty (oily) fish such as anchovies, herring, farmed and wild salmon, sardines, trout, and white tuna tend to have the highest concentrations.39

In vitro and animal experiments suggest that fish oil has direct antiarrhythmic effects,40 but trials to establish direct antiarrhythmic effects in patients with preexisting arrhythmias have been inconsistent.41,42 In human trials, fish oil lowers triglyceride levels,43 systolic and diastolic BP,44 and resting heart rate.45 Observational and RCT evidence suggests that fish or fish oil consumption may also reduce inflammation, improve endothelial function, normalize heart rate variability, improve myocardial relaxation and efficiency, and, at high doses, limit platelet aggregation.46

Consistent with these physiological benefits, habitual fish consumption is associated with lower incidence of CHD and ischemic stroke, especially risk of cardiac death ( Figure 1 ), among generally healthy populations. Compared with no fish consumption, consumption of ~250 mg/d EPA plus DHA from fish is associated with 36% lower CHD mortality.39 Fish and fish oil are among only a handful of dietary factors for which both long-term observational studies and RCTs of CVD outcomes have been performed ( Table 2 ). Four of 8 large RCTs of fish or fish oil, including participants with and without prevalent heart disease, documented significant reductions in CHD events.46 Several of these RCTs had relevant limitations.46 In meta-analyses of RCTs, fish oil supplementation significantly reduced cardiac mortality, including fatal CHD and sudden cardiac death. Overall, these findings are concordant with long-term observational studies of habitual fish intake in generally healthy populations and with physiological benefits of fish or fish oil in intervention studies ( Table 2 ). Whether benefits of eating fish can be fully reproduced by fish oil supplements is not yet established.

Consumption of commercially fried fish or fish sandwiches has not been linked to benefits, possibly because of lower EPA plus DHA content or other added ingredients. Evidence for possible adverse cardiovascular effects of methylmercury found in a few fish species is limited and conflicting; if present, such effects do not appear to outweigh the net cardiovascular benefits of fish consumption.10,54a

Nuts

Nuts contain several bioactive constituents that could improve cardiometabolic health, including unsaturated fatty acids, vegetable proteins (eg, L-arginine, a nitric oxide precursor), fiber, folate, minerals, antioxidants, and phytochemicals.55-57 In RCTs, nut consumption reduces total cholesterol, LDL cholesterol, postprandial hyperglycemia from high-carbohydrate meals, and (variably) oxidative, inflammatory, and endothelial biomarkers. Nut consumption is also associated with less adiposity in observational studies, and in RCTs, the addition of nuts to weight loss diets results in either similar or greater overall weight loss.60 In prospective cohorts, modest nut consumption is associated with lower CHD incidence ( Figure 1 ).61,62 Epidemiological and clinical studies have predominantly evaluated tree nuts and peanuts, and effects of specific types of nuts require further study. Overall, cardiovascular benefits of modest nut consumption are supported by effects on risk factors in short-term trials and by the magnitude and consistency of reduced CVD risk observed in prospective cohort studies ( Table 2 ).

Legumes (eg, peas, beans, lentils, and chickpeas) may also provide cardiovascular benefits. In a meta-analysis of RCTs, consumption of soy-containing foods produced trends toward lowering of systolic (−5.8 mm Hg) and diastolic (−4.0 mm Hg) BP, but effects did not achieve statistical significance.63 Isolated soy protein or isoflavones (phytoestrogens) appear to have smaller effects, producing only modest reductions in diastolic BP (−2 mm Hg) and LDL cholesterol (−3%).63,64 Legumes provide an overall package of micronutrients, phytochemicals, and fiber that could plausibly reduce cardiometabolic risk. Further investigation of their effects in well-conducted prospective cohorts and RCTs is required.

Meats

Several constituents of red meats could increase cardiometabolic risk, including SFA, cholesterol, heme iron, and in processed meats, high levels of salt and other preservatives. Lower consumption of red meats is consistently part of overall dietary patterns associated with lower CVD risk (see "Dietary Patterns" and Table 2 ). In meta-analyses of prospective cohort studies, total red meat consumption was associated with overall nonsignificant trends toward higher risk of CHD and DM ( Figure 1 ).61,65 When different types of meat were evaluated systematically, consumption of processed meats but not unprocessed red meats was associated with higher incidence of CHD and DM.65 These findings suggest that adverse effects of preservatives (eg, sodium, nitrites, and phosphates) and/or preparation methods (eg, high-temperature commercial cooking/frying) could influence health effects of meat consumption.65 In one observational analysis, both unprocessed and processed meat consumption were associated with higher CHD risk when such consumption replaced foods with cardiometabolic benefits, such as low-fat dairy, nuts, and fish.66

Dairy Foods

Some short-term RCTs have evaluated the potential benefits of dairy consumption for satiety or weight loss, with inconsistent and inconclusive findings.67,68 Multicomponent dietary interventions that included daily intake of low-fat dairy foods significantly lowered BP, lipid levels, and insulin resistance and improved endothelial function, independent of changes in weight. In such multicomponent interventions, the specific benefits of dairy foods cannot be quantified separately. Nonetheless, consistent with physiological benefits, higher dairy consumption was associated with lower risk of both stroke and DM in long-term observational cohorts ( Figure 1 ).69-71

The active constituents for such cardiometabolic benefits are not established. On the basis of lower content of calories, SFA, and cholesterol, together with no established nutritional advantage of whole-fat dairy, most dietary guidelines and scientific organizations recommend low-fat or nonfat dairy consumption.10 These guidelines generally recommend dairy foods as a source of selected nutrients (eg, calcium, vitamin D, protein, potassium, magnesium, and other vitamins) rather than based on equally or more relevant evidence for their effects as a whole food that may reduce cardiometabolic risk. In long-term observational studies, a lower risk of DM and metabolic abnormalities has been variably linked to consumption of low-fat dairy, whole-fat dairy, or both.72-77 Conjugated linoleic acid and calcium were proposed as potential mediators, but RCTs have demonstrated very small benefits or even adverse cardiometabolic effects of these factors.78-84 Dairy foods contain a complex assortment of other ingredients that could each play a role in lowering cardiometabolic risk, including specific fatty acids,77 proteins and peptides, vitamins, and other nutrients. Potentially varying health effects of specific dairy foods (eg, milk, yogurt, cheese, and butter) also require further study.85-87a

Sugar-Sweetened Beverages

Evidence from ecological comparisons and prospective cohorts supports positive associations of sugar-sweetened beverage intake with adiposity in children and adults.87a,88 In the United States between 1965 and 2002, when overweight/obesity was increasing rapidly, the proportion of total dietary calories consumed from beverages increased from 11.8% to21.0%, or ~222 calories/d per person.89 Most of this increase was from sugar-sweetened beverages (60%), such as sodas/colas, sweetened fruit drinks, and sports drinks, followed by alcohol (31%) and 100% fruit juices (9%); calories from other beverages (eg, milk) did not increase. The average American teenage boy drinks ~24 oz/d (300 kcal) of sugar-sweetened beverages; the average American teenage girl, ~16 oz/d (200 kcal).90 Most sugar-sweetened beverage intake by children occurs at home, not at school.91

Limited short-term trials suggest that compared with solid foods, calories in liquid form may be less satiating and thereby increase the total amount of daily calories consumed.92,93 Sugar-sweetened beverage intake can also displace more healthful beverages, such as milk.94 Several RCTs of small (n=15) to moderate (n=644) sizes have demonstrated that reduced sugar-sweetened beverage intake improves weight loss or reduces weight gain in both children and adults.88 In one multicomponent lifestyle intervention, each 1-serving/d reduction in sugar-sweetened beverages was associated with 0.65-kg greater weight loss.95 In a meta-analysis of prospective cohorts, higher sugar-sweetened beverage intake was associated with higher incidence of DM and metabolic syndrome.96 One cohort observed a positive association between sugar-sweetened beverage intake and incident CHD.97 The combination of highly refined carbohydrate calories, a liquid form that may minimize satiety, absence of other beneficial nutrients/constituents, displacement of more healthful beverages, and very high intake in many population subgroups renders reduction in sugar-sweetened beverages an important dietary target for improving individual and population cardiometabolic health.

Alcohol

Alcohol use has been related to both beneficial and adverse cardiovascular outcomes. Habitual heavy alcohol intake is cardiotoxic, causing a large portion of nonischemic dilated cardiomyopathies in many nations.98 The ensuing ventricular dysfunction is often irreversible, even when alcohol consumption is stopped; continued drinking in such patients is associated with high mortality. Both acute binges and higher habitual intake of alcohol have also been associated with higher risk of atrial fibrillation.99

Conversely, in controlled trials and in the absence of weight gain, modest alcohol use raises high-density lipoprotein cholesterol, reduces systemic inflammation, and improves insulin resistance.100-102 Consistent with these effects, compared with nondrinkers, individuals who drink alcohol moderately (up to ~2 drinks/d for men and ~1 drink/d for women) experience a lower incidence of CHD and DM.61,103 In these observational studies, benefits of moderate alcohol intake could be overestimated, because the comparison category of nondrinkers often includes former drinkers and other individuals who avoid alcohol because of poor health,104 and because individuals burdened by negative effects of alcohol are generally underrepresented in such long-term studies, for which participation requirements favor healthier individuals. Nonetheless, the consistently lower event rates in observational studies and demonstrated physiological benefits in RCTs provide concordant evidence that moderate alcohol use confers at least some cardiometabolic benefit.

Experimental studies suggest that some nonalcohol components, such as resveratrol in wine, could have potential benefits, but evidence from both RCTs of risk factors and prospective cohort studies of clinical end points are most consistent with direct effects of alcohol itself. For example, moderate intakes of wine, beer, and liquor have each been associated with lower CHD risk in different populations.106 The pattern of drinking appears quite relevant, with lowest cardiovascular risk seen among individuals who drink moderately on several days of the week, rather than among irregular or binge drinkers.107 Because of alcohol-related accidents, homicides, and suicides, especially among younger adults, alcohol use has an overall net adverse effect on population mortality.2 Thus, alcohol use is not advisable as a population-based strategy to reduce CVD risk. For adults who already drink alcohol, no more than moderate use can be encouraged. Avoidance of weight gain should also be reinforced, because an average serving of alcohol contributes ~120 to 200 kcal that, as discussed previously, may be less satiating than calories from solid foods.

Dietary Patterns

An impressive and expanding body of evidence demonstrates that overall dietary patterns can improve health and prevent CVD ( Table 2 ).108 Several healthful dietary patterns have been identified, often derived by different research approaches but sharing several key characteristics, including an emphasis on fruits, vegetables, other plant foods such as beans and nuts, and (in many patterns) whole grains and fish; with limited or occasional dairy products; and often with limited red meats or processed meats and fewer refined carbohydrates and other processed foods ( Table 3 ). These dietary patterns are each generally consistent with food-based priorities for CVD health ( Table 1 ). In RCTs, consumption of such dietary patterns substantially improves multiple cardiovascular risk factors ( Figure 3 ).

Table 3.

Dietary Pattern

DASH (Higher Carbohydrate)

DASH (Higher Monounsaturated Fat)

DASH (Higher Protein)

Traditional Mediterranean (Greece)*

Traditional Mediterranean (Spain)

Mediterranean (US)

Vegetarian

Traditional Japanese

Traditional Okinawan

Citation

Swain et al, 2008109

Swain et al, 2008109

Swain et al, 2008109

Trichopoulou et al, 2003110

Nunez-Cordoba et al, 2009110a

Fung et al, 2009"110b

Craig et al, 2009110c

Willcox et al, 2007111and 2009111a

Willcox et al, 2007111 and 2009111a

Limits (small amounts)

Processed meats

Processed meats

Processed
meats

Meats, dairy

Red meats, sweets

Potatoes

Red meats, poultry

Milk products

Meats, eggs, dairy products

Nutrients/day †

Saturated fat, % energy

6

6

6

13.3

10

10 (Including trans)
‡
2.0

1.9

Foods/day †

Dietary Approaches to Stop Hypertension

DASH (Dietary Approaches to Stop Hypertension) dietary patterns emphasize fruits, vegetables, and low-fat dairy products; include whole grains, poultry, fish, and nuts; and are lower in red meat, sweets, and sugar-sweetened beverages.22,109 The original DASH diet was low in total fat (27% energy) and higher (55% energy) in carbohydrate; additional DASH diet patterns have been evaluated that exchange ~10% energy of carbohydrate for vegetable sources of monounsaturated fat or protein.109 In controlled feeding trials, each of these DASH diets significantly lowered BP and improved blood lipids compared with usual Western diets ( Figure 3 ),22,112 which highlights the greater importance of specific food choices rather than macronutrient composition for maximization of CVD benefits. BP reduction was greatest when DASH diets were combined with reduced sodium intake.22 In multiple observational studies, greater adherence to DASH dietary patterns was associated with lower risk of CVD.10 Unfortunately, very few US adults, even those with elevated BP, currently eat a diet consistent with DASH dietary patterns.113

Mediterranean

Diverse agricultural patterns, cultures, and countries bordering the Mediterranean Sea preclude defining any single Mediterranean dietary pattern or simple criteria. Mediterranean diets have also changed over time: In Crete, a Mediterranean island with historically low rates of CHD, diets now contain less fruit and olive oil and more meats than diets of earlier generations, with associated increases in serum cholesterol and adiposity among these modern residents.114 Still, many traditional Mediterranean diets share common characteristics, including an emphasis on vegetables, fruits, breads/cereal foods usually made from wheat, nuts, and olive oil; sometimes including fish and (in non-Islamic countries) wine with meals; and being lower in saturated fat, cholesterol, and meats.110,115 Ecological comparisons and prospective cohort studies consistently demonstrate inverse associations between consumption of traditional Mediterranean diets and risk of CHD, stroke, and total mortality.116 In RCTs, traditional Mediterranean diets improve several physiological risk factors ( Figure 3 ).

Vegetarian

Several types of vegetarian diets are consumed around the world, including those consumed by pesco-vegetarians (who consume fish); lacto-ovo-vegetarians (who consume milk and eggs); and strict vegans (who consume no animal products). Potentially different cardiometabolic effects of these different vegetarian diets are not established. Few RCTs of vegetarian diets have been performed ( Table 2 ). Two small trials (n=58 and n=20 subjects, respectively) demonstrated reductions in BP with vegetarian diets versus typical Western diets.117,118 Three other trials found no differences between lacto-vegetarian or vegan diets versus conventional dietary recommendations for improving weight loss, BP, blood lipids, or insulin resistance.119-122 In several observational studies, vegetarians experienced improved health outcomes compared with nonvegetarians.10,110a,110b,123,124 Several characteristics of vegetarian diets could account for these relationships, including greater inclusion of plant-based foods and fewer meats, processed meats, and other processed and fast foods.110c Because vegetarians are often generally more health conscious, other lifestyle characteristics, in addition to diet, could contribute to observed lower rates of CVD. Overall, vegetarian diets have been studied less extensively than DASH or Mediterranean patterns, and although the foods that are not consumed (animal products) are their strictly defining feature, the more salient features for CVD benefits may be the foods that are typically consumed, in particular more fruits, vegetables, legumes, nuts, and vegetable oils.25

Japanese

Japanese diets have been of considerable interest, particularly from Okinawa, which until recently experienced among the lowest rates of CHD in the world.111 Traditional Japanese diets emphasize soybean products, fish, seaweeds, vegetables, fruits, and green tea and are low in meats.126 Conversely, Japanese diets often contain high sodium from soy sauce and added salt at home, likely contributing to the relatively high incidence of stroke and some cancers. Very low-fat Japanese diets have also been linked to higher observed stroke risk, including hemorrhagic stroke.127 Food staples of traditional Okinawan diets include orange-yellow root vegetables and green leafy vegetables, which are antioxidant rich and relatively low in calories; wide varieties of seaweeds; tofu; and herbaceous plants.111a Appropriate energy balance and little age-related weight gain are also important features of the Okinawan diet pattern.111 Japanese dietary patterns appear promising for CHD prevention, but the reasons for relatively high rates of stroke and some cancers require further investigation, and epidemiological and clinical trial evidence for benefits remains more limited than evidence supporting the DASH and Mediterranean diets.

Carbohydrate Amount and Quality

Among the most important new insights related to diet and cardiometabolic health is the growing evidence characterizing the importance of carbohydrate quality. Although carbohydrates have traditionally been classified as simple (eg, monosaccharides and disaccharides) versus complex (eg, starch and glycogen), several additional characteristics are relevant in determining cardiometabolic effects. These include dietary fiber content; bran and germ content; food structure (eg, intact, minimally processed, refined, or liquid); and potentially glycemic responses or induction of hepatic de novo lipogenesis following ingestion ( Figure 2 ).

Although the most relevant dimensions of carbohydrate quality, along with a corresponding taxonomy, remain uncertain, it is clear that several aspects of carbohydrate quality influence cardiometabolic health. The effects of dietary fiber are best established, including lowering of serum triglycerides, LDL cholesterol, blood glucose, and BP.31,32 Health effects of bran and germ and food structure have been discussed (see "Whole Grains"). Emerging and compelling evidence suggests that foods with higher glycemic responses can adversely affect blood glucose control and triglycerides and perhaps LDL cholesterol levels, inflammation, endothelial function, and fibrinolysis. Further investigation is needed to establish the clinical relevance and potential independence of such effects from dietary fiber or bran/germ content. Animal experiments and limited human studies suggest that fructose-50% of the sugar in sucrose and 45-55% in high fructose corn syrup-may induce hepatic steatosis and insulin resistance more strongly than glucose.132a Consumption of refined sugars in liquid form appears especially problematic for weight gain (see "Sugar-Sweetened Beverages"). Emerging evidence suggests that the effects of carbohydrate quality may be most relevant in the immediate postprandial period and among individuals more predisposed to insulin resistance.129-132

Whichever metrics are used, it is evident that carbohydrate quality influences cardiometabolic health. Because multiple characteristics appear to be relevant, these health effects are unlikely to be replicated by simple extraction of individual factors (eg, fiber) or nutrients (eg, magnesium) and consumption of these as supplements or food additives.16,17 Important health benefits of consuming energy from higher-quality carbohydrate foods may also relate to substitution, ie, the replacement of more highly refined, lower-quality carbohydrates. Thus, simply eating more whole grains, or consuming individual constituents as supplements, is unlikely to produce the same benefits as substituting whole-grain, higher-quality carbohydrates for refined, lower-quality carbohydrates ( Figure 2 ).

Fat Amount and Quality

Traditionally, dietary recommendations have advised lower total fat intake, primarily because of higher caloric density of fats compared with protein or carbohydrate. However, the type of fats consumed appears to be far more relevant for cardiometabolic health than the proportion of calories consumed from total fat. Calorie for calorie, industrially produced trans fats from partially hydrogenated vegetable oils have the strongest adverse relations with CHD risk,136 and consumption of such fats should be as close to zero as possible.10 Conversely, seafood-derived omega-3 PUFAs have strong inverse relations with CHD mortality,39,46 and a recent World Health Organization Expert Consultation recommended that all adults consume at least 250 mg/d EPA plus DHA from seafood.11 Some evidence supports cardiovascular benefits of plant-derived omega-3 fats, but compared with naturally occurring omega-3 from seafood, the potency of plant-based omega-3 appears weaker, and mixed findings preclude strong conclusions.137,138

On the basis of animal experiments, ecological comparisons, and RCTs documenting effects on LDL cholesterol,139 greater SFA consumption has traditionally been associated with increased CHD risk. Conversely, 3 recent meta-analyses of all available prospective observational studies found that individuals consuming the highest amounts of SFA had a similar incidence of CVD events as those consuming the lowest amounts. Although the reasons for these conflicting results remain controversial, growing evidence suggests that cardiometabolic effects of SFA consumption are modified by which nutrients (or foods) are decreased or increased in exchange for SFA ( Table 2 ). For example, in most prospective observational studies, SFA consumption was compared with the average background diet, which in these studies was often heavily composed of less healthful refined carbohydrates that induce their own adverse cardio-metabolic effects (see above).

Several lines of evidence support this explanation. In pooled individual-level data from 11 observational cohorts, consumption of PUFA was associated with lower CHD risk than SFA, as would be expected.142 However, SFA consumption, traditionally considered highly atherogenic, had relatively similar associations with CHD risk as total carbohydrate, the most common (calorically predominant) background macronutrient.142 Similar effects of SFA and carbohydrates on the ratio of total to HDL cholesterol have been documented, and may contribute to this finding. Overall carbohydrate quality and fiber content (as well as underlying predisposition to insulin resistance) would be expected to modify the relative effects of SFA vs. carbohydrate. In a recent observational analysis, SFA consumption was associated with a trend toward higher CHD risk than low-glycemic, higher-fiber (eg, whole grain) carbohydrates and with lower CHD risk when it replaced high-glycemic (eg, highly refined) carbohydrates.145 On the basis of these findings and high proportions of refined carbohydrates in most diets, a focus on reducing SFA consumption, traditionally a major public health goal, needs to be paired with decreasing consumption of refined carbohydrates, starches, and sugars.141,144 More explicitly, recommendations to replace SFA with PUFA (see below) and replace refined carbohydrates/starches and sugars with less refined, higher-fiber carbohydrate foods are relevant ot reducing cardiometabolic risk.10 The importance of prioritizing healthier food choices is especially clear ( Table 1 ). Although different individual SFAs (eg, palmitic acid or stearic acid) have different effects on blood lipids, current evidence is insufficient to determine whether these individual SFAs have differential effects on disease outcomes.144 The health effects of many other individual fatty acids also require further study. Limitations in dietary assessment methodology persist, and advances in such methods in combination with use of objective biomarkers will enable more definitive investigation of these and related questions.

Cardiovascular effects of total PUFAs, largely derived from certain vegetable oils (eg, soybean, safflower, and corn), have been evaluated extensively. PUFA consumption improves levels of blood lipids and lipoproteins, is associated with lower CVD event rates in prospective cohort studies, and reduces clinical events as a replacement for SFA in RCTs. Consumption of monounsaturated fatty acids has been shown to favorably affect levels of blood lipids and lipoproteins,139 improved insulin resistance in some but not other RCTs,146-148 and was related to lower CVD risk (when consumed from vegetable oils) in ecological studies.149 However, because consumption of monounsaturated fatty acids has been shown to increase atherosclerosis in nonhuman primates150 and has mixed relations with clinical CVD events in long-term cohort studies, some caution is needed.61,142 Also, because monounsaturated fat is derived from both animal (eg, meats and dairy) and vegetable (eg, olive oil, and canola) sources, health effects may plausibly vary depending on the types of foods consumed. For example, potential adverse effects of saturated fat, cholesterol, heme iron, or preservatives in meats could counter cardiometabolic benefits,65 whereas potential effects of phenolic compounds in olive oil could augment benefits.151 Thus, consumption of vegetable oils, including those that contain PUFA, plant-derived omega-3 fats, and MUFA, is an important feature of dietary patterns that reduce CVD risk ( Table 1 ).

Sodium

Animal experiments, migration studies, ecological studies, longitudinal observational studies, RCTs, and meta-analyses confirm that higher salt (sodium chloride) consumption raises BP.152 Elevated BP is estimated to account for nearly two thirds of strokes and half of all CHD events.153 Individual large-scale trials and meta-analyses of trials have documented conclusively that several different BP-reduction therapies prevent stroke and CHD.154 This compelling body of evidence has led numerous organizations to conclude that salt reduction, through its effects on BP, should likewise prevent stroke and CHD.10,13 A meta-analysis of prospective observational studies supports a direct relationship between increased salt intake and CVD events.155 Limited evidence from trials, including long-term follow-up of salt-reduction trials, is also consistent with lower CVD event rates after salt reduction.156,157

In North America and Europe, 75% of sodium intake is derived from packaged, preprepared, or restaurant foods, with the rest being naturally occurring or added at home.158 In Asian countries, most sodium is from soy sauce or is added at home.158 Given ubiquitous sources of sodium in American and similar diets ( Figure 4 ),159 policy-level approaches are well-suited for reduction efforts. Projected benefits are enormous. A national effort that reduced US salt intake by 3 g/d (~1.2 g/d less sodium) could annually prevent between 60 000 and 120 000 CHD events and 32 000 to 66 000 strokes, saving 194 000 to 392 000 quality-adjusted life-years and $10 to $24 billion in healthcare costs.160 Smaller reductions in salt intake are also estimated to produce large population benefits.160,161 Overall, the totality of evidence supports aggressive policy-level approaches to lower sodium intake as a means to prevent the CVD consequences of elevated BP. Optimal BP reduction occurs when sodium reduction is combined with a healthier food-based dietary pattern such as the DASH-type diet ( Table 1 ).

Dietary Supplements

Use of dietary supplements, often at high or pharmacological doses, is commonplace, despite the absence of convincing evidence that supplements have health benefits. Several supplements have been evaluated in observational studies and RCTs as potential therapies to prevent CVD or other conditions ( Table 4 ).46,84,162-166 Evaluated doses have often exceeded usual or even recommended dietary intakes, often under the presumptions that the greater the intake, the greater the benefit, and that risk of harm was negligible. However, substantial evidence has accrued that most of these supplements have few CVD benefits and that certain supplements, including β-carotene, calcium, and vitamin E, can even be harmful. Presently, only omega-3 PUFA can be recommended as a supplement for CVD prevention; optimal doses and target populations require further study. Overall, the current evidence does not support supplementary vitamin or other supplement approaches, including food fortification, to duplicate the cardioprotective benefits of consumption of healthful foods.

Table 4.

Beta-carotene

Some cohort studies have linked low serum levels or low dietary intake of beta-carotene with higher CVD risk. RCTs of beta-carotene supplements document no benefit in the general population and increased risk of lung cancer in patients who were at high risk of lung cancer.162

Calcium

Calcium supplementation with vitamin D3 is recommended as a means to prevent osteoporosis, especially in women. A recent meta-analysis of RCTs suggests that calcium supplementation may increase the risk of myocardial infarction.84

Vitamin D

Emerging evidence from observational studies suggests that low serum vitamin D levels are associated with higher risk of CVD events. RCTs of vitamin D supplementation have not shown conclusive reductions in risk of CVD.163 Additional trials using higher doses of vitamin D supplementation are ongoing.

Vitamin E

Several prospective cohort studies have linked vitamin E consumption or supplementation with lower risk of CHD. RCTs have failed to show reductions in CVD events with supplemental vitamin E, and 2 meta-analyses suggest that high-dose vitamin E supplements may increase total mortality.162,164

Folic acid, vitamin B6, vitamin B12

Observational studies have associated low folate intake, low serum folate levels, and high homocysteine levels with higher risk of CVD outcomes. RCTs have confirmed that folic acid supplementation lowers blood homocysteine levels. Long-term RCTs have not documented benefits of folic acid with or without vitamin B6 and vitamin B12 on CVD outcomes. In some trials, supplemental folic acid was associated with increased risk of CVD.165

Fish oils

Multiple cohort studies have documented an inverse relationship between fish intake and subsequent CHD, in particular CHD death.39 A meta-analysis of larger and multiple smaller RCTs, largely in higher-risk populations, demonstrated a reduction in total mortality with fish oil supplementation.39 Four of 8 large RCTs among patients with and without preexisting CVD demonstrated reductions in CHD events; several of these trials had potentially relevant limitations.46

Multivitamins

Although some cohort studies have observed lower CVD risk with multivitamin supplements, 5 RCTs, rated to be of fair to poor quality, have not documented any clear CVD benefit of multivitamin use in mixed populations.166

Energy Balance

Energy balance (calories consumed versus expended) is the principal determinant of weight gain and adiposity. Basal and activity-related energy expenditure are determined by physical activity, body size, muscle mass, age, and sex. Appropriate energy consumption (total dietary calories per day) is determined by energy expenditure and goals for weight loss, gain, or stability. Some people may consume relatively high calories but have neutral or negative energy balance because of high expenditure, whereas others may consume relatively few calories but have positive energy balance because of low expenditure. Thus, change in weight (supplemented with waist circumference), rather than direct measurement of energy expenditure or consumption, is the most practical metric to assess energy balance.

Whether macronutrient composition (percent energy from total fat, carbohydrate, or protein) has an effect on energy balance was tested recently in RCTs. In early studies not designed to test weight loss, participants assigned to low-fat diets who also received intensive dietary counseling experienced greater short-term weight loss than control subjects who received no dietary counseling.167,168 However, RCTs designed to investigate weight loss and having equal-intensity interventions in each dietary arm have demonstrated that macronutrient composition has little independent effect on weight loss.169-172 Adherence to any weight loss diet, regardless of its macronutrient composition, was the best determinant of success.169-172 Long-term ad libitum dietary trials168 and prospective cohort studies173-175 support that macronutrient composition has little effect on long-term weight gain.

In contrast, behavioral factors, including lower intakes of fruits, vegetables, and whole grains; larger portion sizes; and greater intakes of sugar-sweetened beverages, processed snacks, energy-dense foods, fast food meals, and possibly trans fat, appear to have a greater influence on body weight.87a,88,136,176-181 Thus, these features of dietary quality appear to impact dietary quantity.

Other individual, social, and environmental factors are also linked to energy imbalance. These include television watching and lower average sleep duration, especially among children/adolescents; socioeconomic status and race/ethnicity; local environments, such as the presence of fast food restaurants, grocery stores, crime safety, parks or open spaces, and walking or biking paths; and influences of advertising, social norms, and work and home dynamics. Ultimately, these influences act through changes in diet or activity to influence weight change. For example, effects of television watching and poor sleep may be mediated predominantly by dietary changes.185-190 Although the quality of available time-trend data is suboptimal, the recent obesity pandemic appears temporally related to increased energy consumption in developed nations90 and to both increased consumption and decreased expenditure in some developing nations.3

A sustained energy imbalance of ~50 to 100 extra kcal/d may be enough to produce the weight gain observed in many individuals.191,192 The often small size of this "energy gap" makes unintentional gradual weight gain easy, but also means that small improvements in energy balance, sustained over the long term, could prevent or even reverse adiposity in many individuals and populations.87a,193

Changing Behavior

A growing body of literature supports several effective strategies for successful behavior change.194-197 Evidence for individual-level approaches was reviewed recently ( Table 5 ).197 Targeted goals are most effective for individuals.196,197 Clinical providers can help patients prioritize the most relevant foods and dietary patterns ( Table 1 ) and perform simple office-based assessments to inquire about and help set dietary goals.198 Clinic-based strategies are facilitated by healthcare systems changes, including scheduled visits for individual/group education; sustained in-person, telephone, or electronic feedback; and quality and reimbursement guidelines that support behavior-change efforts.199,200

Table 5.

Cognitive-behavioral strategies

Class I

Goal Setting: Target dietary behaviors with specific, proximal goals.

Feedback: Provide feedback on progress toward goals.

Self-Monitoring: Provide strategies for self-monitoring.

Follow-Up: Establish a plan for frequency and duration of follow-up contacts (eg, in-person, oral, written, electronic) in accordance with individual needs to assess and reinforce progress toward goal achievement.

Motivational Interviewing: Use motivational interviewing strategies, particularly when an individual is resistant or ambivalent about behavior change.

Self-Efficacy: Incorporate strategies to build self-efficacy into the intervention. Combination Strategies: Use a combination of 2 or more of the above strategies in an intervention.

Class IB

Long-Term Support: Provide direct or peer-based long-term support and follow-up, such as referral to ongoing community-based programs, to offset the common occurrence of declining adherence over time.

Class IIB

Use incentives, modeling, and problem-solving strategies.

Intervention processes and/or delivery strategies

Class IA

Individual Sessions: Use individual-oriented sessions to assess where the individual is in relation to behavior change, to jointly identify the goals for risk reduction or improved cardiovascular health, and to develop a personalized plan to achieve it.

Group Sessions: Use group sessions with cognitive-behavioral strategies to teach skills to modify the diet to provide role modeling and positive observational learning, and to maximize the benefits of peer support and group problem solving.

Class IB

E-Programs: For appropriate target populations, use Internet- and computer-based programs to target behavior change, preferably including E-counseling and feedback.

Class IIA

Individualized Print/Media: For print- or media-only strategies, use individualized (rather than nonindividualized) approaches.

Strategies to address cultural and social context

Class IIA

Multicomponent: Use a multiple-component delivery strategy that includes both individual and group components.

Cultural Adaptation: Use culturally adapted strategies, including use of peer or lay health advisors to increase trust, as well as tailored health messages and counseling strategies sensitive to cultural beliefs, values, language, literacy, and customs of the individual.

Class IIB

Settings: Use work, community, church, or clinic settings for delivery of interventions.

Problem Solving: Use problem-solving strategies to address barriers such as lack of access to healthier foods, lack of knowledge related to cooking or food preparation, or transportation barriers.

Although individual-based strategies can successfully improve an individual's diet quality, public health strategies at community, state, and national levels are essential to produce a substantial and sustained population impact.196,201 Several approaches are effective ( Table 6 ).152,196,202-214 Given the scope of prevailing adverse dietary patterns, population approaches are critical to achieving the AHA's 2020 Strategic Goals.7 Overall, although more research on the best translational strategies is needed, sufficient evidence presently exists to implement several individual- and population-level approaches to improving diet.

Table 6.

Policies directly targeting selected nutrients to increase or reduce levels in
foods152,202

Direct mandates or bans

Coordinated, multicomponent media, education, and labeling

Changes in the food environment196,203-209

Increasing availability of healthier foods, eg, in cafeterias, grocery stores, or neighborhoods

Changes in food pricing by means of subsidies or taxation

Point-of-purchase prompts and education

Media and other educational strategies196,210-212

Intensive mass media campaigns promoting one simple message

National logos or simple branding to identify healthier foods †

Provision of focused, targeted messages as part of a larger multicomponent strategy

Regulation of advertising to particular at-risk groups

Posting of information on food labels or menu boardst

Social and community supports196

Coordinated educational and environmental efforts in schools, workplaces, community centers, and religious centers

Group sessions and self-monitoring strategies

Multicomponent strategies196,211,213

Combinations of upstream policy measures, midstream environmental approaches and media campaigns, and downstream community approaches

Conclusions

High-quality evidence is now available from multiple complementary research paradigms on the cardiometabolic effects of specific dietary factors, offering new and expanded insights into dietary priorities for preventing CVD and DM. Consumption of specific foods and dietary patterns appear especially beneficial ( Table 1 ) and warrant a focus on foods and diet patterns appear especially beneficial ( Table 1 ) and warrant a focus on foods and overall dietary patterns rather than individual nutrients or supplements. This focus should also help counter food industry manipulation of nutrient targets (eg, promotion of highly processed, "nutrient-fortified" foods/beverages). An approach based on foods and dietary patterns can also minimize paradoxical choices that may arise from single-nutrient approaches, such as avoiding nuts or vegetable oils because of concerns about SFA or total fat content while instead consuming processed low-fat deli meats, highly refined cereals/breads, and fat-free sugary desserts.6 Levels of selected individual nutrients in foods, such as sodium and industrially produced trans fats, can be efficiently reduced by strong policy strategies. Appropriate energy balance is also essential, which will require sustained approaches that target dietary quality (types of foods/beverages consumed), portion sizes, television watching, physical activity, and local environments.

Although gaps in knowledge remain, a substantial knowledge base informs relevant dietary priorities and behavior-change strategies for improving cardiometabolic health. Effective approaches are required to harness the interest and energy of policy makers and the food industry to improve diet throughout the world. Although many diet-related prevention strategies are likely to be highly cost-effective for society, most policy makers and medical systems remain focused on downstream treatments that use drugs, devices, and surgeries. New strategic initiatives are needed to draw together all key stakeholders-the public, healthcare providers, food industry, and policy makers-to identify remaining barriers and develop operational plans to translate our considerable knowledge on the health effects of foods and dietary patterns and on behavior change into actual improvements in diet.

Acknowledgments

Supported by the National Heart, Lung, and Blood Institute, with cofunding from the Office of Dietary Supplements (R01-HL-085710), National Institutes of Health. We thank Dr Frank Sacks for his critical reading of and comments on an earlier version of this report.

Disclosures

Dr Mozaffarian reports receiving research grants from Glaxo-SmithKline, Sigma Tau, Pronova, and the National Institutes of Health for an investigator-initiated, not-for-profit clinical trial of fish oil; travel reimbursement, honoraria, or consulting fees from the International Life Sciences Institute, Uni-lever, SPRIM, Nutrition Impact, and Foodminds; and royalties from UpToDate for an online scientific chapter. Harvard University has filed a provisional patent application, assigned to Harvard University, listing Dr. Mozaffarian as a co-inventor to the US Patent and Trademark Office for use of trans-palmitoleic acid to prevent and treat insulin resistance, type 2 diabetes, and related conditions. The other authors report no conflicts.

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Components of a Cardioprotective Diet New Insights

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Circulation. Author manuscript; available in PMC 2018 Nov 28. Published in final edited form as: The global burdens of cardiovascular diseases (CVD), type 2 diabetes mellitus (DM), and obesity are rising, producing enormous losses of life and disability-adjusted life-years in both developed and developing nations.1 Most of these burdens are preventable and are occurring at unnecessarily younger ages, largely owing to suboptimal lifestyle, which includes poor diet quality, excess caloric intake, physical inactivity, and smoking.2-5 Worldwide, striking differences in dietary habits and rates of chronic diseases exist.

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Joe Devine: Effects of e-cigarettes and vaping devices on cardiac and pulmonary physiology

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Joe Devine: Effects of e-cigarettes and vaping devices on cardiac and pulmonary physiology

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Vaping has been advertised as a healthier alternative to smoking cigarettes. It has promised users that this is a quicker, healthier, and safer route to quitting smoking. This study is a literature review of multiple studies that looked at the effect of e-cigarettes on the physiological changes of the heart and lungs when exposed to the smoke from vaping. The studies reviewed showed an increase in cardiac heart rate and blood pressure in humans. In the animal models they showed an increase in arterial stiffening, plaque formation, and angiogenesis. The physilogical changes in the lungs showed an increase airway obstruction, airway inflammation, and reactivity.

The chemical additives market for electronic cigarettes is an unregulated wild west. It allows for modification and backyard chemists to make their own concoctions far from safety guidelines. This lack of oversight lead to an INCREASE in harmful chemicals then what is seen in cigarette smoke.

Tsai M, Byun MK, Shin J, Crotty Alexander LE. Effects of e-cigarettes and vaping devices on cardiac and pulmonary physiology. J Physiol. 2020 Nov;598(22):5039-5062. doi: 10.1113/JP279754. Epub 2020 Oct 12. PMID: 32975834.

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The Mediterranean Diet and Cardiovascular Health

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The Mediterranean Diet and Cardiovascular Health

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Clarisa Williams
Consuming a healthy diet is one of the cardio respiratory health metrics proposed by the American Heart Association. There are many benefits of consuming a Mediterranean diet outside of cardio respiratory health but the consumption of the nutritional guidelines for this diet has seen to be beneficial in reducing the rates of cardiovascular disease. The Mediterranean diet consists of low to non-processed foods, reduced red meat consumption, increased oil consumption, and increased non-processed fruit and vegetable consumption. This clinical review evaluated and number of Dietary guidelines listed under the Mediterranean diet and its role in cardiovascular health. One of the findings from the study involve the consumption of polyphenol rich foods that fall under the mediterranean diet criteria. The use of extra-virgin olive oil in the Mediterranean diet is reported to have benefits in reduction of cardiovascular disease. Polyphenols have anti-inflammatory properties. The consumption of extra-virgin olive oil which have higher quantities of bioactive polyphenol which is responsible for the    cardiovascular benefits. This is connected to nutritional science as one of the specific nutritional interventions for improvement cardio vascular health would be to consume a Mediterranean diet along with increased use of extra-virgin olive oil. When providing recommendations in the clinical setting a suggestion of changing the overall diet can be beneficial with cardiovascular health overall. The recommendation of that specific diet can be a means of management and preventative health.
Martínez-González, M. A., Gea, A., & Ruiz-Canela, M. (2019). The Mediterranean diet and cardiovascular health: A critical review. Circulation research, 124(5), 779-798.

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Added Sugar Intake and Cardiovascular Diseases Mortality Among US Adults

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Added Sugar Intake and Cardiovascular Diseases Mortality Among US Adults

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Posted by Richard Proudfoot

The research paper selected for this week is titled: “Added Sugar Intake and Cardiovascular Diseases Mortality Among US Adults” This April 2014 article was published in the Journal of American Medical Association Internal Medicine.  The authors collaborated from the Division for Heart Disease and Stroke Prevention, Centers for Disease Control and Prevention, Atlanta, Georgia (Yang, Zhang, Merritt); Division of Diabetes Control, Centers for Disease Control and Prevention, Atlanta, Georgia (Gregg); Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia (Flanders); Department of  Nutrition, Harvard School of Public  Health, Boston, Massachusetts (Hu);  Department of Epidemiology,  Harvard School of Public Health,  Boston, Massachusetts (Hu).

This association study used a prospective cohort of a nationally representative sample of US adults of the National Health and Nutrition Examination Survey (NHANES, 1988-1994, 1999-2004, and 2005-2010) and NHANES III Linked Mortality cohort, to examine time trends of added sugar consumption as percentage of daily calories in the United States and investigate the association of this consumption with cardiovascular disease (CVD) mortality.

This study is important because Americans consume a large part of their calories from added sugar sources, particularly sugar sweetened beverages.  Most adults (71%) consume 10% or more calories from added sugar.  The authors observed a significant relationship between added sugar consumption and increased risk for CVD mortality.

The key findings from this study are that most US adults consume more added sugar than is recommended for a healthy diet. A higher percentage of calories from added sugar is associated with significantly increased risk of CVD mortality. In addition, regular consumption of sugar-sweetened beverages is associated with elevated CVD mortality.  Adjusted hazard ratios were 1.30  and 2.75, respectively, comparing participants who consumed 10.0%to 24.9% or 25.0%or more calories from added sugar with those who consumed less than 10.0%of calories from added sugar.

Clinical implication of this study support current recommendations to limit the intake of calories from added sugars in US diets.1 Since the majority of Americans do not follow the current recommendations to limit sugar consumption, we need to educate the public to limit their added sugar consumption.  Society may choose to tax added sugar to discourage over consumption.  And public information campaigns could create a stigma against added sugars just as we have created a stigma against fats, trans fats and cholesterol.

Yang Q, Zhang Z, Gregg EW, Flanders WD, Merritt R, Hu FB. Added sugar intake and cardiovascular diseases mortality among US adults. JAMA Intern Med. 2014;174(4):516-524. doi:10.1001/jamainternmed.2013.13563

https://doi.org/10.1001/jamainternmed.2013.13563

Posted by Richard Proudfoot

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Cardiovascular Disease in Racial/Ethnic Minority Populations- Cole Cincinelli

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Cardiovascular Disease in Racial/Ethnic Minority Populations- Cole Cincinelli

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By 2023, 130 million Americans or 46% of the United States population are projected to have some form of cardiovascular disease(CVD) according to the American Heart Association.  CVD can be predisposed in family genetics or developed from multiple risk factors. These risk factors include Tobacco use, hypertension, high cholesterol, physical inactivity, and diabetes. The food availability and healthcare access could impact the development of these risk factors and consequently CVD. “Structural and psychosocial obstacles including insurance burden, limited access to care, lack of provider cultural competency, health illiteracy, English language barriers, and stress secondary to discrimination contribute to an increase in CVD risk factors and consequent CVD”(Muncan, 2018). Ethnic minority poses a unique difficulty in the proper management of diagnosed CVD and comorbidities for these reasons and leads to greater cardiovascular-cause mortality, compared to White counterparts(Muncan, 2018). This is important for physicians to be aware of. They should include operations to be more inclusive to all patients. Some physicians offices and even hospitals should implement an electronic translating system to overcome language barriers and advertise more towards minority groups. Physicians should keep this in mind when they are assessing these patients and developing a treatment plan, being aware of the availability to their patient. Collectively this could help slow the increased rate of cardiovascular disease in the United States.

Muncan B. Cardiovascular disease in racial/ethnic minority populations: illness burden and overview of community-based interventions. Public Health Rev. 2018;39:32. Published 2018 Dec 3. doi:10.1186/s40985-018-0109-4

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The Fluid Aspect of the Mediterranean Diet in the Prevention and Management of Cardiovascular Disease and Diabetes: Ashley Wahlman

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The Fluid Aspect of the Mediterranean Diet in the Prevention and Management of Cardiovascular Disease and Diabetes: Ashley Wahlman

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An article that struck my interest this week, was an article discussing the benefits of red wine and olive oil for treating atherosclerosis. As mentioned in this paper, low-moderate consumption of red wine has been shown to play a role in the prevention of cardio vascular diseases. This article, discusses how phenols which is a compound present in red wine and olive oil may slow the atherogenic process by inhibiting oxidative damage and restoring endothelial function. This relates to nutritional science due to the fact that red wine and olive oil are predominantly present in a Mediterranean diet, which is a diet that is becoming more popular. I think this has great clinical implications. Possibly by educating patients on how certain foods may help to prevent CVD or atherosclerosis may eventually lead to fewer patients developing these issues down the line. Also, it allows the patient to take charge in their health and if they are more pre disposed to CVD changing their diet at least to the fluid intake present in a Mediterranean diet might be a good idea. Also, I think it is important to note that clinicians would need to preface the low-moderate consumption of red wine. It doesn't take a lot to see the benefits and if too much is consumed as we know might result in alcohol related liver disease.

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The Fluid Aspect of the Mediterranean Diet in the Prevention and Management of Cardiovascular Disease and Diabetes: The Role of Polyphenol Content in Moderate Consumption of Wine and Olive Oil - PubMed

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A growing interest has emerged in the beneficial effects of plant-based diets for the prevention of cardiovascular disease, diabetes and obesity. The Mediterranean diet, one of the most widely evaluated dietary patterns in scientific literature, includes in its nutrients two fluid foods: olive oil,…