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Healthy Dietary Patterns Defense against Cardiovascular Disease and Diabetes

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Clinical Nutrition".

Deadline for manuscript submissions: closed (25 January 2025) | Viewed by 4538

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Guest Editor
Department of Translational Research, Western University of Health Sciences, Pomona, CA 91766, USA
Interests: vascular inflammation; immunomodulation; remodeling; thrombosis; atherosclerosis; neoangiogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

“We Are What We Eat” by Alice Waters suggests that diet plays a critical role in our physiological, psychological, and mental health. Unhealthy dietary patterns, including a high salt or high cholesterol diet, together with a lack of exercise, overweight and obesity, aging, gender, genetics, vitamin D deficiency, or a smoking habit, are risk factors for and contribute towards cardiovascular disease (CVDs), including atherosclerosis, coronary artery disease, myocardial infarction, and stroke. Diets including higher amounts of processed meat, sugar, and refined grains are associated with greater CVD incidence, while moderate coffee and alcohol intake, and high fruit/vegetable, low-fat dairy, whole grain, fish, and nut intake are associated with lower incidence. Diabetes is a risk factor for CVD, and the intake of saturated fat and sugars is associated with a higher incidence of diabetes. This suggests that an unhealthy diet is a risk factor for metabolic syndrome, increasing the risk of coronary heart disease, diabetes, stroke, and other serious health problems. Thus, it is important to follow a healthy diet with exercise to decrease the risk of diabetes, CVDs, and other health issues.

I proudly announce this Special Issue of Nutrients, entitled “Healthy Dietary Patterns Defense against Cardiovascular Disease and Diabetes”, where we invite the submission of multidisciplinary projects, including original and review articles related, but not limited to, the association of diet with atherosclerosis, coronary artery disease, stroke, and metabolic syndrome; geographical area and risk of CVDs; and dysbiosis and metabolic syndrome.

Dr. Vikrant Rai
Guest Editor

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Keywords

  • cardiovascular disease
  • diabetes
  • overweight
  • healthy diet
  • metabolic syndrome

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Published Papers (3 papers)

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Research

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13 pages, 270 KiB  
Article
The Influence of Lifestyle Factors on Resting Energy Expenditure and Its Role in Cardiometabolic Risk: A Cross-Sectional Study
by Joanna Ostrowska and Dorota Szostak-Węgierek
Nutrients 2025, 17(6), 1044; https://doi.org/10.3390/nu17061044 - 16 Mar 2025
Viewed by 649
Abstract
Objectives: This cross-sectional study aimed to examine the associations between lifestyle factors (diet, physical activity, and sleep) and resting energy expenditure (REE) in a group of 75 healthy adults aged 30–45 years without obesity, and to explore its relationship with body composition parameters [...] Read more.
Objectives: This cross-sectional study aimed to examine the associations between lifestyle factors (diet, physical activity, and sleep) and resting energy expenditure (REE) in a group of 75 healthy adults aged 30–45 years without obesity, and to explore its relationship with body composition parameters and selected biochemical markers that could positively influence cardiometabolic disease prevention. Methods: For this purpose, indirect calorimetry, accelerometers, and bioelectrical impedance analysis (BIA) were used. Results: We found that fat-free mass (FFM) showed the strongest association with REE, along with related metrics such as total body water, body cell mass, and muscle mass (p < 0.0001, adj. R2 > 0.5). In univariable models, all physical activity intensities were significantly associated with REE, but only moderate physical activity (MPA) remained significant after adjusting for sex and FFM (β = 2.1 ± 1.0, p < 0.05, adj. R2 = 0.589). Similarly, a positive association between HDL-C and REE persisted after adjustments (β = 4.8 ± 2.3 kcal/d, p < 0.05, adj. R2 = 0.590). Further analyses confirmed that MPA and HDL-C independently contributed to REE (ΔR2 = 0.02, p < 0.05; Partial r = 0.233 and 0.236, respectively, both p < 0.05), highlighting their role beyond the effects of FFM and sex. Other biochemical and lifestyle factors, including HOMA-IR, insulin levels, triglycerides, and total energy intake, showed positive associations with REE in the crude model. However, these relationships diminished after adjustment, suggesting that their influence is likely mediated by factors such as body composition, body size, and sex. Finally, no significant relationship between sleep and REE was observed in our cohort under naturalistic conditions, possibly due to the alignment of participants’ sleep durations with recommended guidelines. Conclusions: These potential direct links between MPA–REE and REE-HDL may be partially explained by habitual, spontaneous physical activity, which contributes to post-exercise metabolic elevation and may promote adipose tissue browning, potentially resulting in favorable metabolic effects, that support cardiometabolic disease prevention. Full article

Review

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17 pages, 1150 KiB  
Review
High-Fat Diet, Epigenetics, and Atherosclerosis: A Narrative Review
by Vikrant Rai
Nutrients 2025, 17(1), 127; https://doi.org/10.3390/nu17010127 - 31 Dec 2024
Cited by 1 | Viewed by 1928
Abstract
Background/Objectives: Atherosclerosis is a chronic inflammatory disease developing and progressing in the presence of risk factors including hyperlipidemia, hypercholesterolemia, and chronic inflammation, among others. Atherosclerosis commonly precipitates as ischemic events, transient ischemic attacks, and myocardial infarction. Saturated fatty acids are risk factors; however, [...] Read more.
Background/Objectives: Atherosclerosis is a chronic inflammatory disease developing and progressing in the presence of risk factors including hyperlipidemia, hypercholesterolemia, and chronic inflammation, among others. Atherosclerosis commonly precipitates as ischemic events, transient ischemic attacks, and myocardial infarction. Saturated fatty acids are risk factors; however, their association with epigenetics in the pathophysiology of atherosclerosis is not clearly understood. The preclinical and clinical trials associating atherosclerosis with epigenetics are scarcely documented, and most of the studies reported the use of drugs inhibiting methylation and histone modification to improve atherosclerosis. This narrative review aims to discuss various aspects and the association between a high-fat diet, epigenetic reprogramming, and atherosclerosis. Methods: A literature search with the keywords high-fat diet, epigenetics, and atherosclerosis, alone or in combination, was conducted to search for articles in the English language. Duplicate articles were removed, and articles related to the subject of this review article were included in this review. Results: A review of the literature suggests that a high-fat diet with saturated fatty acids is a risk factor for atherosclerosis, but this association is multifactorial, and epigenetics play a critical role. However, the connecting link and the underlying molecular and cellular mechanisms are not clearly understood yet and warrant more research. Conclusions: A high-fat diet rich in saturated fatty acids is a risk factor for atherosclerosis involving epigenetic reprogramming and altered gene expression. The existing preclinical and clinical trials support the role of epigenetics and reversing it using drugs to attenuate atherosclerosis, but definitive evidence warrants larger clinical trials. Further, a high-fat diet in pregnant mothers can manifest as cardiovascular disease in offspring; caution must be taken in pregnant mothers for their diet and nutrients. Full article
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Other

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9 pages, 1376 KiB  
Brief Report
A High-Fat Diet Induces Epigenetic 1-Carbon Metabolism, Homocystinuria, and Renal-Dependent HFpEF
by Suresh C. Tyagi
Nutrients 2025, 17(2), 216; https://doi.org/10.3390/nu17020216 - 8 Jan 2025
Cited by 1 | Viewed by 1468
Abstract
Background/Objectives: Chronic gut dysbiosis due to a high-fat diet (HFD) instigates cardiac remodeling and heart failure with preserved ejection fraction (HFpEF), in particular, kidney/volume-dependent HFpEF. Studies report that although mitochondrial ATP citrate lyase (ACLY) supports cardiac function, it decreases more in human HFpEF [...] Read more.
Background/Objectives: Chronic gut dysbiosis due to a high-fat diet (HFD) instigates cardiac remodeling and heart failure with preserved ejection fraction (HFpEF), in particular, kidney/volume-dependent HFpEF. Studies report that although mitochondrial ATP citrate lyase (ACLY) supports cardiac function, it decreases more in human HFpEF than HFrEF. Interestingly, ACLY synthesizes lipids and creates hyperlipidemia. Epigenetically, ACLY acetylates histone. The mechanism(s) are largely unknown. Methods/Results: One hypothesis is that an HFD induces epigenetic folate 1-carbon metabolism (FOCM) and homocystinuria. This abrogates dipping in sleep-time blood pressure and causes hypertension and morning heart attacks. We observed that probiotics/lactobacillus utilize fat/lipids post-biotically, increasing mitochondrial bioenergetics and attenuating HFpEF. We suggest novel and paradigm-shift epigenetic mitochondrial sulfur trans-sulfuration pathways that selectively target HFD-induced HFpEF. Previous studies from our laboratory, using a single-cell analysis, revealed an increase in the transporter (SLC25A) of s-adenosine–methionine (SAM) during elevated levels of homocysteine (Hcy, i.e., homocystinuria, HHcy), a consequence of impaired epigenetic recycling of Hcy back to methionine due to an increase in the FOCM methylation of H3K4, K9, H4K20, and gene writer (DNMT) and decrease in eraser (TET/FTO). Hcy is transported to mitochondria by SLC7A for clearance via sulfur metabolomic trans-sulfuration by 3-mercaptopyruvate sulfur transferase (3MST). Conclusions: We conclude that gut dysbiosis due to HFD disrupts rhythmic epigenetic memory via FOCM and increases in DNMT1 and creates homocystinuria, leading to a decrease in mitochondrial trans-sulfuration and bioenergetics. The treatment with lactobacillus metabolites fat/lipids post-biotically and bi-directionally produces folic acid and lactone–ketone body that mitigates the HFD-induced mitochondrial remodeling and HFpEF. Full article
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