Dietary Approaches to Prevent Hypertension

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

Deadline for manuscript submissions: 5 July 2024 | Viewed by 956

Special Issue Editor


E-Mail Website
Guest Editor
1. Department of Pharmacology, Center for Biomedical Research (CIBM), University of Granada, 18071 Granada, Spain
2. Instituto de Investigación Biosanitaria de Granada (ibs. GRANADA), 18012 Granada, Spain
Interests: immune system; gut microbiota; trained immunity; cardiovascular disease; probiotics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Hypertension is one of the most powerful risk factors for cardiovascular events, including stroke and myocardial infarction. Around one-quarter of the world’s population is considered hypertensive, and this condition is responsible for about 41% of cardiovascular disease-related deaths. Treatment using antihypertensive drugs can reduce the risk of major cardiovascular events. Currently, it is estimated that 10–30% of the general hypertensive population presents with resistant hypertension, which is defined as high BP that cannot be adequately controlled using three different classes of antihypertensive agents, one of which is a diuretic. These data support the need for the development of novel therapeutic targets for hypertension.

Recently, an imbalance in the gut microbiota composition relative to its healthy state, termed dysbiosis, has been associated with hypertension; however, the mechanisms involved in BP regulation that are controlled by the microbiota have not yet been fully elucidated. It is essential to maintain the delicate balance in the gut microbiota to achieve intestinal immunity and whole-body homeostasis. Therefore, manipulating the gut microbiota through dietetic manipulation or the use of probiotics, prebiotics, or postbiotics may lead to the development of novel antihypertensive therapies.

This Special Issue will focus on basic and translational research and clinical evidence to achieve complete comprehension of how modulating the gut microbiota is involved in hypertension. Research will also consider the role of the immune system and the sympathetic nervous system.

Dr. Iñaki Robles-Vera
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • gut microbiota
  • cardiovascular disease
  • diet
  • probiotics
  • prebiotics

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

14 pages, 616 KiB  
Article
Dietary Fructose and Sodium Consumed during Early Mid-Life Are Associated with Hypertensive End-Organ Damage by Late Mid-Life in the CARDIA Cohort
by Dragana Komnenov, Mohammad Al-Hadidi, Hamza Ali, Malik Al-Jamal, Kassim Salami, Samy Shelbaya, Kareem Tayeb, Daniel Domin and Rana Elhamzawy
Nutrients 2024, 16(7), 913; https://doi.org/10.3390/nu16070913 - 22 Mar 2024
Viewed by 803
Abstract
We aimed to investigate how dietary fructose and sodium impact blood pressure and risk of hypertensive target organ damage 10 years later. Data from n = 3116 individuals were obtained from the Coronary Artery Risk Development in Young Adults (CARDIA) study. Four groups [...] Read more.
We aimed to investigate how dietary fructose and sodium impact blood pressure and risk of hypertensive target organ damage 10 years later. Data from n = 3116 individuals were obtained from the Coronary Artery Risk Development in Young Adults (CARDIA) study. Four groups were identified based on the four possible combinations of the lower and upper 50th percentile for sodium (in mg) and fructose (expressed as percent of total daily calories). Differences among groups were ascertained and logistic regression analyses were used to assess the risk of hypertensive target organ damage (diastolic dysfunction, coronary calcification and albuminuria). Individuals in the low-fructose + low-sodium group were found to have lower SBP compared to those in the low-fructose + high-sodium and high-fructose + high-sodium groups (p < 0.05). The highest risk for hypertensive target organ damage was found for albuminuria only in the high-fructose + high-sodium group (OR = 3.328, p = 0.006) while female sex was protective across all groups against coronary calcification. Our findings highlight that sodium alone may not be the culprit for hypertension and hypertensive target organ damage, but rather when combined with an increased intake of dietary fructose, especially in middle-aged individuals. Full article
(This article belongs to the Special Issue Dietary Approaches to Prevent Hypertension)
Show Figures

Figure 1

Back to TopTop