Abstract
Background:
Cancer therapies induce cardiac injury and increase cardiovascular disease (CVD) risk. In non-cancer populations, higher diet quality is associated with protection against CVD, but the relationship between diet and cardiac function in cancer survivors is unknown.
Methods:
This cross-sectional analysis from the Multi-Ethnic Study of Atherosclerosis (MESA) cohort included 113 cancer survivors (55 breast, 53 prostate, three lung, and three blood) and 4,233 non-cancer controls. Dietary intake was reported via validated food frequency questionnaire. Alternate healthy eating index (AHEI) was calculated as a measure of quality. Cardiac function, determined as left ventricular ejection fraction (LVEF), was assessed by cardiac magnetic resonance.
Results:
Cancer survivors had a lower LVEF compared to controls (61.3 ± 6.5% v 62.4 ± 6.1%, p=0.04). In all participants, total fat (β ± SE: −0.04 ± 0.01, p=0.004), saturated fat (−0.11 ± 0.03, p<0.001), and trans-fat (−0.36 ± 0.12, p=0.002) intake were inversely associated with LVEF while AHEI (0.03 ± 0.01, p<0.001) was positively associated with LVEF. Among cancer survivors only, sucrose intake was negatively related to LVEF (−0.15 ± 0.06, p=0.02), and ratio of unsaturated fat to saturated fat (2.7 ± 1.1, p=0.01) and fiber intake (0.42 ± 0.14, p=0.003) were positively related to LVEF.
Discussion:
In cancer survivors, improved dietary fat and carbohydrate quality (i.e., greater consumption of unsaturated fatty acids and fiber) was associated with favorable cardiac function, while higher sucrose was associated with worse cardiac function. Further research is needed to confirm these findings and test whether changes in the identified dietary factors will modulate cardiac function in cancer survivors.
Keywords: cancer survivors, diet, unsaturated fatty acids, fibers, cardiac function
INTRODUCTION
Early detection and improved medical treatments have greatly increased 5-year cancer-related survival rates (1). Unfortunately, these treatments also cause cardiovascular (CV) injury including cardiomyocyte damage, valvular disease, arrhythmias, pericardial disease, and coronary disease (2). Cancer treatment-related cardiac injury places cancer survivors at high risk for long-term left ventricular (LV) dysfunction, exercise intolerance, progressive fatigue, and CV disease (CVD) events—including the risk for heart failure (HF) (3–7). Cancer therapy-related cardiac dysfunction is often measured as a reduction in LV ejection fraction (LVEF) in cancer survivors, making LVEF an optimal marker for evaluating cardiac function in this population(8). The emergence of CVD events among cancer survivors threatens to offset the progress in cancer-related survival achieved through adjuvant therapies. Yet, there are currently no therapies routinely administered in this population to address declines in cardiac function and resultant high risk of HF.
In non-cancer populations, strong evidence demonstrates that greater adherence to a healthy diet pattern, characterized by high consumption of vegetables, fruits, whole grains, lean proteins, and vegetable oils, reduces an individual’s risk for CVD mortality by 22%(9). Moreover, data from randomized controlled trials show that dietary interventions aimed at improving quality of dietary fats by consuming foods rich in unsaturated fatty acids (UFA) can result in significant reduction in CVD in both primary and secondary prevention(10,11). Additionally, poor diet quality can also increase the risk of developing overweight, obesity, and deposition of visceral adipose tissue(12), which are shared risk factors for the development of CVD and cancer(13), and may increase risk of CVD in cancer survivors (14). However, inconsistencies in findings suggest a greater complexity in the relationship between obesity and cancer that is inadequately understood(13).
To date, there are no studies that characterize dietary intake related to cardiac function in cancer survivors, and whether measures of adiposity might augment such relationship. Indeed, there is a lack of data to inform evidence-based clinical nutrition guidelines that may mitigate risk of cardiac dysfunction in this population. To that end, the aim of this study was to leverage an existing dataset to examine the associations between dietary intake, dietary quality, and cardiac function in cancer survivors and non-cancer controls, and test if adiposity attenuated or moderated these relationships among cancer survivors.
METHODS
This is a secondary analysis of the Multi-ethnic Study of Atherosclerosis (MESA) cohort, which has been previously described in detail(15). Briefly, the aim of MESA was to extensively phenotype a large cohort of racially diverse participants in the United States to study the progression of subclinical CVD. Participants included in the current study had complete data from the cancer history question, diet history survey (food frequency questionnaire), anthropometry, and cardiac magnetic resonance (CMR) imaging at baseline/examination 1 study visit (Supplemental Figure 1). Baseline/examination 1 data was used to ensure that no participants were undergoing treatment for cancer at the time of data collection. Cancer survivorship was obtained from questionnaires collecting data on medical history, including history of cancer. Individuals who indicated a history of breast, lung, prostate, or blood cancer were coded as cancer survivors. Those who reported no history of cancer were coded as non-cancer participants. Individuals who indicated a history of colon cancer, “other” cancer type, or type 1 diabetes were excluded from the study due to the possible impact on dietary patterns and food choices. Additionally, individuals who indicated a history of nonmelanoma skin cancer were excluded due to the superficial nature of the cancer. Finally, individuals who responded “don’t know” for cancer history were also excluded. The final sample size included in the study was 4,346 participants. Demographic, socioeconomic status, medical history, and medication use data were collected from participants at the baseline study visit.
Dietary Intake and Quality
Habitual dietary intake was assessed via a food frequency questionnaire that was previously validated in a racially diverse population(16). For the MESA study, the questionnaire was modified to include foods commonly consumed by people of Chinese descent as well as additional information for whole grains, processing of plant foods, and flavonoids(15). Individuals with reported intakes above 6,000 calories (kcal) or below 500 kcal were considered implausible and were excluded from analyses. Gram intakes of dietary variables were adjusted per 1000 kcal intake. The ratio of unsaturated fatty acids (UFA) to saturated fatty acids (SFA) was calculated as a measure of dietary fat quality. The alternate healthy eating index (AHEI) was calculated as a measure of total dietary quality(17). AHEI was computed as described by McCullough et al. (17) except the dietary fiber variable was based on total dietary fiber with an intake of 30 g per day considered optimal(18).
Cardiac Function
Cardiac function was measured using CMR imaging on 1.5 T scanners as previously described, including reliability measures(15,19). Electrocardiogram gating was used for CMR imaging, and blood pressure was monitored from the brachial artery. Fast gradient echo cine images were collected of the left ventricle with <50 msec time resolution. Readings were completed at one location (Department of Radiology, Johns Hopkins University School of Medicine) using MASS software (version 4.2, Medis, The Netherlands). LVEF was considered the primary measure of cardiac function for this study due to the importance of LVEF in detecting cancer-therapy related cardiotoxicity(8). Cardiac assessments of LV-end diastolic volume index (mL/m2), LV-end systolic volume index (mL/m2), stroke volume index (mL/m2), and LV mass index (g/m2) were also included. In a subset of the cohort, strain relaxation index (SRI) was also used as a measure of diastolic function (20).
Anthropometry and Clinical Assessment
Body mass index ( BMI ;kg/m2) was calculated from height measured to the nearest 0.1 cm and weight measured to the nearest 0.5 kg. Waist circumference was assessed at each participant’s umbilicus and recorded to the nearest 0.1 cm. Blood pressure was assessed by an automated method (Dinamap) in the right arm following five minutes of rest. Three measurements were taken, and the second and third measures were averaged for reporting.
Statistical Analyses
All continuous measures were summarized as mean ± standard deviation, and categorical measures were summarized as count and percentage. Dietary intake information was described as grams/1000 kcal or percent of total calories. The unadjusted association between dietary intake and dietary quality variables and LVEF were examined using simple linear regression. Potential confounders (age, race/ethnicity, sex, income, education, physical activity, smoking history) were tested both conceptually and statistically by estimating the correlation coefficients between each dietary intake variable and potential confounders, performing partial F-tests, and fitting linear regression models with and without each potential confounder. Variables were considered confounders if parameter estimates changed by 10% or more when added to the model.
Multiple linear regression analyses with selected confounders (i.e., age, race/ethnicity, education) were used to test for the differences in dietary intake and dietary quality variables between cancer survivors and non-cancer participants. Multiple linear regression analyses were also used with selected confounders (i.e., age, sex, race/ethnicity, smoking history) to test for the relationship between dietary variables and LVEF. To test for differences between cancer survivors and non-cancer participants in the diet-cardiac function relationships, cancer status was included as a main effect and as an interaction term with cancer status and the dietary variable. For select variables where the cancer status-dietary variable interaction term was statistically significant, participants were categorized as reporting above or below the median intake of the diet variable and LVEF was compared between participants above or below the median intake, adjusting for age, race/ethnicity, sex, and smoking history. Similar analyses to those described for LVEF were conducted with additional measures of cardiac function (LV end diastolic volume, LV end systolic volume, LV mass, stroke volume, and SRI). Strain relaxation index was log-transformed to account for a non-normal distribution. To test if adiposity attenuated the diet-cardiac function association, BMI was added to regression models as a covariate. To test if adiposity moderated the relationship between dietary variables and cardiac function, an interaction term between dietary variables and BMI was added to regression models stratified by cancer status. Interaction effects were considered significant at p<0.1.
RESULTS
Baseline Characteristics
Cancer participants were older than control participants (Table 1, p<0.001), and there was a difference in distribution of race between the groups (p=0.01). Women represented about half of the cohort for cancer and control participants. Among cancer participants, there were 55 breast cancer survivors, 53 prostate cancer survivors, three lung cancer survivors, and three blood cancer survivors. One individual reported history of both prostate and lung cancer. Thirteen percent of cancer participants were current smokers, which was similar to 12% of control participants (p=0.11). A greater proportion of the cancer group was taking blood-pressure lowering medications (p<0.001), but there was no difference in proportion of participants with type 2 diabetes mellitus (p=0.10) or taking lipid-lowering medication (p=0.85). Systolic blood pressure was higher among cancer survivors compared to control participants (p=0.02), but diastolic blood pressure was not different between groups (p=0.89). BMI (p=0.61) and waist circumference (p=0.16) were similar between groups.
Table 1.
Demographic and clinical characteristics of participants with and without a history of cancer
| Characteristic | Control Participants (n = 4,233) | Cancer Participants (n = 113) | p-value |
|---|---|---|---|
| Age (years) | 61.2 ± 10.0 | 69.1 ± 8.2 | <0.001 |
| Race/Ethnicity | 0.01 | ||
| White | 1615 (38) | 51 (45) | |
| Black | 1066 (25) | 37 (33) | |
| Hispanic | 967 (23) | 17 (15) | |
| Chinese | 585 (14) | 8 (7) | |
| Sex | 0.87 | ||
| Female | 2188 (52) | 57 (50) | |
| Male | 2045 (48) | 56 (50) | |
| Cancer History | |||
| Breast Cancer | 55 (49) | ||
| Prostate Cancer | 53 (47) | ||
| Lung Cancer | 3 (3) | ||
| Blood Cancer | 3 (3) | ||
| Smoking Status | 0.11 | ||
| Current | 527 (12) | 15 (13) | |
| Former | 1494 (35) | 50 (44) | |
| Never | 2206 (52) | 48 (43) | |
| Blood-pressure Lowering Medication | <0.001 | ||
| Yes | 1467 (35) | 61 (54) | |
| No | 2765 (65) | 52 (46) | |
| Diabetes* | 0.10 | ||
| Yes | 419 (10) | 17 (15) | |
| No | 3811 (90) | 96 (85) | |
| Lipid-lowering Medication | 0.85 | ||
| Yes | 663 (16) | 19 (17) | |
| No | 3562 (84) | 94 (83) | |
| Systolic Blood Pressure (mm Hg) | 125.2 ± 21.1 | 130.1 ± 18.2 | 0.02 |
| Diastolic Blood Pressure (mm Hg) | 72.0 ± 10.3 | 72.1 ± 10.7 | 0.89 |
| Body Mass Index (BMI, kg/m2) | 27.7 ± 4.9 | 27.5 ± 4.6 | 0.61 |
| Waist Circumference (cm) | 96.4 ± 13.2 | 98.2 ± 12.8 | 0.16 |
| Cardiac Function and Structure | |||
| Left ventricular ejection fraction (%) | 62.4 ± 6.1 | 61.3 ± 6.5 | 0.04 |
| LV-end diastolic volume index (mL/m2) | 68.4 ± 12.7 | 65.7 ± 12.3 | 0.03 |
| LV-end systolic volume index (mL/m2) | 25.7 ± 6.9 | 25.3 ± 5.9 | 0.51 |
| LV mass index (g/m2) | 63.8 ± 11.7 | 64.2 ± 11.9 | 0.66 |
| LV stroke volume index (mL, m2) | 42.7 ± 8.6 | 40.4 ± 9.1 | 0.006 |
| Log(Strain relaxation index) (ms/%) | 0.76 ± 0.62 | 0.80 ± 0.66 | 0.71 |
Values are presented as mean ± standard deviation or n (%).
Among control group, n=4227 for smoking status and diabetes status, n=4232 for anti-hypertensive medications, and n=1245 for strain relaxation index
Among cancer survivors group, n=40 for strain relaxation index
Among cancer group, one participant reported history of both prostate and lung cancer.
Abbreviations: LV, left ventricular
LVEF was lower among cancer survivors than control participants (p=0.04). LV-end systolic volume index, LV mass index, and strain relaxation index were similar between groups. LV end diastolic volume index and stroke volume index were lower among cancer survivors compared to control participants (p=0.03 and p=0.006, respectively).
Dietary Intake and Cardiac Function
There were no statistically significant differences in dietary intake or measures of diet quality between cancer survivors and controls (Table 2). Participants in both groups reported similar intakes of calories from fat, carbohydrates, and protein as reported in both grams/1000 kcal and percentage of total energy intake. Total dietary quality assessed by AHEI was similar between groups.
Table 2.
Dietary intake and dietary quality in participants with and without a history of cancer
| Dietary Variable | Control Participants (n= 4,233) | Cancer Participants (n= 113) | p-value |
|---|---|---|---|
| Total Energy (kcal) | 1,597 ± 13 | 1,556 ± 74 | 0.59 |
| Total Fat (% total kcal) | 29.9 ± 0.1 | 30.0 ± 0.6 | 0.84 |
| Saturated fat (% total kcal) | 9.7 ± 0.1 | 9.8 ± 0.3 | 0.64 |
| Unsaturated fat (% total kcal) | 18.5 ± 0.1 | 18.6 ± 0.4 | 0.92 |
| Trans fat (% total kcal) | 0.77 ± 0.01 | 0.74 ± 0.03 | 0.43 |
| Total Fat (g/1000 kcal) | 33.2 ± 0.1 | 33.4 ± 0.7 | 0.84 |
| Saturated Fat (g/1000 kcal) | 10.7 ± 0.1 | 10.9 ± 0.3 | 0.64 |
| Unsaturated Fat (g/1000 kcal) | 19.5 ± 0.1 | 19.5 ± 0.42 | 0.96 |
| Trans Fat (g/1000 kcal) | 1.9 ± 0.01 | 1.9 ± 0.1 | 0.43 |
| UFA:SFA ratio | 2.1 ± 0.01 | 2.0 ± 0.1 | 0.59 |
| Total Carbohydrates (% total kcal) | 54.5 ± 0.1 | 54.1 ± 0.8 | 0.71 |
| Sucrose (% total kcal) | 9.2 ± 0.1 | 9.4 ± 0.4 | 0.57 |
| Total Carbohydrate (g/1000 kcal) | 136.2 ± 0.4 | 135.4 ± 2.1 | 0.71 |
| Sucrose (g/1000 kcal) | 22.9 ± 0.2 | 23.5 ± 0.9 | 0.57 |
| Total Fiber (g/1000 kcal) | 12.3 ± 0.1 | 12.1 ± 0.4 | 0.71 |
| Total Protein (% total kcal) | 16.0 ± 0.1 | 16.2 ± 0.3 | 0.51 |
| Total Protein (g/1000 kcal) | 40.0 ± 0.1 | 40.5 ± 0.8 | 0.51 |
| Alternate healthy eating index | 44.1 ± 0.2 | 43.2 ± 1.1 | 0.45 |
Values are represented as adjusted mean ± standard error of the mean. Data are adjusted for age, race/ethnicity, and education.
UFA: unsaturated fatty acids; SFA, saturated fatty acids
In all participants, associations between dietary intake variables and LVEF are shown in Table 3. Total fat was inversely related to LVEF in all participants (β ± SE: −0.03 ± 0.01, p=0.005). By type of fat, SFA were inversely associated with LVEF (−0.12 ± 0.03, p<0.001) while UFA were not associated with LVEF (−0.01 ± 0.02, p=0.47). Trans-fat intake was also inversely related to LVEF (−0.36 ± 0.12, p=0.003). The interaction term between UFA:SFA and cancer status was significant at p<0.1 (−1.04 ± 0.5, p=0.04), and analyses were carried out stratified by cancer status. Among cancer survivors, individuals with an UFA:SFA intake above the median exhibited higher LVEF values compared to those below the median (64.0 ± 0.9 vs. 58.9 ± 0.9, p<0.001, Figure 1A). There was also a positive association between UFA:SFA (2.6 ± 1.1, p=0.02) and LVEF (Figure 1B). The non-cancer group demonstrated a similar positive association between UFA:SFA (0.72 ± 0.16, p<0.001) with LVEF. There was also a statistically significant interaction between cancer status and sucrose intake (0.06 ± 0.03, p=0.02). Among cancer survivors, participants with a sucrose intake below the median had an LVEF of 62.8% ± 0.9 compared to an LVEF of 60.5% ± 1.0 in participants above the median of sucrose intake (Figure 1C, p=0.057). Additionally, sucrose intake was negatively related to LVEF in the cancer group (−0.13 ± 0.06, p=0.04, Figure 1D); however, among non-cancer controls, sucrose intake was not associated with LVEF (−0.01 ± 0.009, p=0.26). The interaction term between cancer status and fiber intake was also statistically significant (−0.14 ± 0.06, p=0.03). Cancer participants with a fiber intake above the median had a higher LVEF relative to those below the median fiber intake (63.2 ± 0.9 vs. 60.1 ± 1.0, p=0.01, Figure 1E). Total fiber intake was positively related to LVEF in both cancer survivors (0.42 ± 0.14, p=0.003, Figure 1F) and non-cancer controls (0.07 ± 0.02, p=0.002). Overall diet quality assessed by AHEI was also positively associated with a higher LVEF (0.03 ± 0.01, p<0.001). All associations between dietary intake and LVEF remained statistically significant following additional adjustment for BMI. Of note, BMI was not a moderator of any relationships between diet and LVEF among cancer survivors. Results of associations between dietary intake and additional measures of cardiac function are shown in supplemental table 1.
Table 3.
Results from multiple linear regression with dietary variables as the predictor and left ventricular ejection fraction (LVEF, %) as the response among all participants
| Dietary Variable | β ± standard error | p-value |
|---|---|---|
| Total Fat (g) | −0.03 ± 0.01 | 0.005 |
| Saturated Fatty Acids (g, SFA) | −0.12 ± 0.03 | <0.001 |
| Unsaturated Fatty Acids (g, UFA) | −0.01 ± 0.02 | 0.47 |
| Trans Fat (g) | −0.36 ± 0.12 | 0.003 |
| UFA:SFA ratio | 0.77 ± 0.16 | <0.001 |
| Total Carbohydrate (g) | 0.008 ± 0.004 | 0.06 |
| Sucrose (g) | −0.01 ± 0.01 | 0.12 |
| Total Fiber (g) | 0.08 ± 0.02 | <0.001 |
| Total Protein (g) | 0.006 ± 0.01 | 0.60 |
| Alternate healthy eating index | 0.03 ± 0.01 | <0.001 |
Dietary variables were adjusted as g/1000 kcal intake. Beta estimates and standard errors are presented from fully adjusted models with age, sex, race/ethnicity, and smoking history included as covariates.
Figure 1.
Panels A, C, and E: Differences in left ventricular ejection fraction (LV EF) for cancer survivors above and below median intake of unsaturated fatty acid to saturated fatty acid ratio (UFA:SFA), sucrose intake, and fiber intake. Panels B, D, and F: Relationships between intake of UFA:SFA, sucrose, and fiber and LVEF among cancer survivors with beta estimates and standard errors shown on each graph. All data are adjusted for age, race, sex, and smoking history.
DISCUSSION
In cancer survivors, indicators of diet quality were associated with cardiac function, particularly systolic function as determined by LVEF. Specifically, greater diet quality (i.e., higher AHEI score), and particularly dietary fats quality (i.e., greater UFA:SFA, lower SFA and trans-fats), and carbohydrates quality (i.e., more fiber and lower sucrose) were associated with a greater LVEF. These data provide initial evidence that dietary quality correlates with cardiac systolic function in cancer survivors at high risk for CVD and CVD complications.
Quality of fat and carbohydrate intake was linked to cardiac function in this cohort of cancer survivors. Higher dietary quality is associated with a lower risk of CVD(21); however, less research has focused on dietary quality linked to measures of cardiac function and the underlying mechanisms driving this relationship. Preclinical mechanistic studies suggest that unhealthy dietary patterns (i.e., Western diet) high in SFA and sucrose, can directly induce cardiac dysfunction in mice(22). Of note, our group has shown that the Western diet-induced cardiac dysfunction can be reversed by improved diet quality(22), and even prevented by modulating the quality of the fatty acids through increasing the consumption of UFA, without changing total energy and total fat intake (23). Moreover, we and others have shown that such effects are largely mediated by the pro-inflammatory cytokines interleukin (IL)-1 and IL-18, both products of the NLRP3 (nod like receptor protein-3) inflammasome, which is thought to play a key role in cardiac remodeling(24–26). This has been further confirmed in human studies, where a meal rich in SFA and sugars resulted in increased circulating pro-inflammatory cytokines, particularly of IL-18(27). Conversely, UFA are a well-known modulator of inflammation and have been shown to inhibit the activation of the NLRP3 inflammasome(28,29). UFA consumption was also associated with favorable cardiovascular function measures including cardiorespiratory fitness in patients with heart failure(23,30). Together, these data demonstrate a potential mechanism by which quality of fat and carbohydrate intake may be linked to cardiac function in cancer survivors, but research is needed to confirm this relationship in this population.
In addition, results herein suggest that greater saturated fat and trans-fat intake may be associated with worsening cardiac function regardless of cancer history, and among cancer survivors, higher UFA intake may promote better cardiac function. While a healthful, nutrient-dense diet will contain foods with SFA, nutrition recommendations center around limiting SFA and exchanging SFA intake for UFA intake for reduced CVD and mortality risk(31–33). These recommendations are supported by findings presented here in which among cancer survivors, higher intake of UFA relative to SFA was associated with better LVEF. Moreover, a study of breast cancer survivors reported that participants in the highest quintile or SFA and trans-fat intake had higher mortality risk than those in the lowest quintile of intake (34), although cardiac function was not assessed. In the current study, intake of trans-fats was also associated with lower LVEF. Trans-fat consumption induces inflammation, arrhythmias, endothelial dysfunction, and metabolic dysregulation including insulin resistance (35). Trans-fat intake is also related to higher mortality risk (36), and limiting or eliminating trans-fats consumption is recommended by numerous health organizations (31,33,37). Together, these findings suggest the quality of dietary fat may play a role in influencing cardiac function in those with and without a cancer history.
Quality of carbohydrate intake, namely higher fiber consumption and lower sucrose intake, was also associated with better LVEF among cancer survivors. Sucrose and fiber intake have health implications beyond cardiac systolic function relevant to cancer survivors. Intake of foods high in sucrose, such as sugar-sweetened beverages, are associated with an increased risk of developing atherosclerosis and a higher CVD mortality rate (38,39). Sugar-sweetened beverages are also a concern for cancer incidence and recurrence as a higher consumption of these beverages is linked to higher risk of overweight and obesity(33). Conversely, diets high in fiber are characterized by foods with lower energy density but high in nutrients, thereby helping individuals keep a healthy body weight, lessen stress on the CV system, and further reduce CVD risk(13,33). Little work has been done testing for mechanisms, such as inflammation, linking diet and CV function. Clinical trials in cancer survivors are urgently needed to investigate the role of diet and inflammation on CV health and function, and if dietary prescription may lessen inflammation tied to cardiac injury.
CVD and cancer share some overlapping risk factors, such as obesity(13). The relationship between obesity and breast cancer, for example, is multifaceted and not fully understood. We hypothesized that adiposity may moderate the relationships between diet and cardiac function; however, this was not found to be true in this population using measures of BMI. Overall healthfulness of lifestyle may confer benefits against disease regardless of BMI. In breast cancer survivors, adherence to healthy lifestyle behaviors, including fruit and vegetable consumption and physical activity participation, was linked to a 50% reduction in mortality risk, regardless of obesity(40). However, it is important to consider that specific fat depots exert varying metabolic effects(41), and assessing adiposity and fat distribution by more accurate methods may yield different results and further insight into the relationships between adiposity, diet, and cardiac function in cancer survivors.
Several limitations exist for this study. The cross-sectional study design was used to ensure no cancer participants were actively receiving treatment during study assessments. However, this study design precludes inference of a cause-and-effect relationship between diet and cardiac function. Cancer survivors who were free of clinically recognized CVD and enrolled in MESA may not be representative of all cancer survivors, and this study includes a heterogenous cohort of cancer survivors. The data available to discern cancer history and type of cancer did not include stage of cancer or treatment received, including chemotherapy, type of chemotherapy, surgery, or radiation. This limitation prevents investigation into the specific treatments administered to participants. Nevertheless, this study provides evidence of associations between dietary intake and heart function in cancer survivors and controls.
In conclusion, dietary intake may help mitigate the high risk of CVD in cancer survivors, but there is a lack of evidence to guide clinical practice. This study reports that higher diet quality, including quality of dietary fatty acids and carbohydrates, was associated with cardiac function in cancer survivors. Further research is needed to confirm these associations, and to determine the underlying mechanisms by which diet may preserve cardiac function in cancer survivors at high risk of CVD.
Supplementary Material
Acknowledgements:
We gratefully acknowledge the MESA study participants, staff, and investigators.
Funding:
Funding for this study was provided by grants from the National Institutes of Health, National Cancer Institute (T32CA093423). Services and products in support of the research project were generated by the VCU Massey Cancer Center Biostatistics Shared Resource, supported, in part, with funding from NIH-NCI Cancer Center Support Grant P30 CA016059. This research was supported by contracts 75N92020D00001, HHSN268201500003I, N01-HC-95159, 75N92020D00005, N01-HC-95160, 75N92020D00002, N01-HC-95161, 75N92020D00003, N01-HC-95162, 75N92020D00006, N01-HC-95163, 75N92020D00004, N01-HC-95164, 75N92020D00007, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168 and N01-HC-95169 from the National Heart, Lung, and Blood Institute, and by grants UL1-TR-000040, UL1-TR-001079, and UL1-TR-001420 from the National Center for Advancing Translational Sciences (NCATS). The authors thank the other investigators, the staff, and the participants of the MESA study for their valuable contributions. A full list of participating MESA investigators and institutions can be found at http://www.mesa-nhlbi.org. This paper has been reviewed and approved by the MESA Publications and Presentations Committee.
Abbreviations:
- AHEI
alternate healthy eating index
- BMI
body mass index
- CMR
cardiac magnetic resonance
- CV
cardiovascular
- CVD
cardiovascular disease
- HF
heart failure
- IL
interleukin
- LVEF
left ventricular ejection fraction
- MESA
multiethnic study of atherosclerosis
- NLRP3
nod-like receptor protein-3
- SFA
saturated fatty acids
- SRI
strain relaxation index
- UFA
unsaturated fatty acids
Footnotes
Data Share Statement: Data described in the manuscript, code book, and analytic code will be made available upon request pending MESA publications and presentations committee approval.
Disclosures: The authors have no disclosures relevant to the work.
Conflict of interest: None.
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