How gut health shapes heart disease risk — and what you can do about it

From gut bacteria to bullying heart disease-researchers have revealed how your microsum can be the next border to prevent cardiovascular problems.

Study: Beyond the intestine: Eliminating the multi -dimensional influence of micro -biochem on cardiovascular health. Image Credit: Shutter Stock AI Generator / Shutter Stock.com

In a recent research published in Clinical Nutrition AspinResearchers, researchers examine the role of gut microbium in maintaining cardiovascular health.

Cardiovascular disease vs chronic kidney disease

Cardiovascular disease (CVD) is an important cause of death worldwide. Former diagnosis of diabetes, hypertension, or disclipidia, some medicines, and lifestyle factors such as smoking, drinking, dietary quality, and lack of exercise can increase the risk of CVD growth.

Chronic kidney disease is also widely found all over the world, diagnosing the disease with 10 % of people. Chronic disease of the kidney varies, some people maintain their kidney function despite the end -stage kidney disease damage. Like CVD, the risk of chronic kidney disease also increases in the presence of obesity, diabetes and hypertension.

The joint role of hypertension

Hypertension is a major risk for both kidney disease and CVD. Salt consumption is the most common factor that increases, causes hypertension.

Salt, which is otherwise known as sodium chloride, is an ionic mixture that is primarily absorbed through the intestinal mucosa. The use of more foods in salt can lead to microscoal endoral inflammation, morphological regeneration and active problems.

Some parts of the population are particularly sensitive to the effects of salt, as their blood pressure levels may change in response to the amount of salt, while others may not be affected by these foods. Salt sensitivity can be caused by the genetic polymorphism of the presence of the Rainy-Enogrendor-uldosterone System (RAAS), nutrient intake, or the presence of kidney disease.

Cardiovascular illness and gut microbiome

SCFS

Short chain (SCFA) manufactured by Gut Microscopic through various receptors, organizes blood pressure, which meet with GPR 41, GPR 43, and Wilfrethri GPR 78 (OLFR 78). Activating these receptors leads to nitric oxide (NO) preparation and RAAS regulation, both of which cause vasodity.

The share of acetate, proportionate, and the partnership is 60 %, 20 %, and 20 % of the total SCFA production of Gut Microbium. However, changing the synthesis of gut microsum can reduce the production of SCFA, thus increasing the chances of hypertension condition.

SCFA is very important to maintain the integrity of intestinal obstruction through the effects of their inflammation on both colonial epithelial and immune cells, using Rudent hypertension models. For example, the Bhyrite stabilizes hypoxia-inducible factor-1 (HIF-1), which reduces blood pressure levels and further secures the functioning of the bowel obstruction by reducing its permeability.

tmao

The high circulating levels of gut metabulite traymithin n oxide (TMAO) can lead to aortic stiffness, thus increasing the risk of cystolic blood pressure and CVDs. High -fat diets such as red meat, milk and fish are often rich in phosphatedellocin, choline, and L Carnetine, all of which are trumpets (TMA) and TMAO advance molecules.

The increase in the amount of salt can also cause high plasma levels of TMAOs, which can lead to atrosclerosis, non -fatal microidal infections, hypertension and stroke. Recent animal studies have reported that an enzyme contained in TMAO synthesis, the experimental pressure of the Flavin -containing monotensionis 3 (FMO 3), a significant reduction in the formation of ethroscalotric plaque and improves cholesterol metabolism.

The release of TMAO in systemic circulation can lead to oxidation of lipoprotein (LDL), which can prevent effective vasodilation. Oxidized LDL can lead to high levels of cholesterol -1, causing vocational and hypertension.

The TMAO is also considered an inflammatory substance, as its release produces the production of oxygen species (ROS) and inflammatory pro -cytokines, both of which cause vascular inflammation and endometal discipline.

Lipopolisacroid

Lipopolisacroid (LPS) is manufactured during gut dysbuses, which is caused by imbalance in the proportion of pathogenic from beneficial bacteria in the gut micro -biochemos. Once released in the systemic circulation, the LPS can attract inflammation by binding a toll-like receptor 4 (TLR4), which can lead to the preparation of pro-inflammatory cytiqins such as pro-inflammatory cytikines such as Intein 6 (IL-6), IL-1, IL-27, and tumor-neurosis element.

Treating CVD through a balanced gut microbiome

The use of pre -biotics, probiotics, and dietary modifications, which aims to re -establish balanced gut micro -biota, can promote SCFA production and reduce TMAO levels.

Pre -biotics, which promote the development of beneficial bacteria in the gut, and probiotics, which provide beneficial bacteria to the gut, have been investigated for their ability to acquire homeistosis in the gut microsum and promote cardiovascular health. However, additional studies are needed to determine the effectiveness of these treatments, as published studies report mixed results.

A balanced diet, considerable physical activity, and stress management is key to maintaining a healthy gut microbiome. In this way, intervention that makes these lifestyle easier can be effective in reducing the risk of CVD.

The Faculty Microbiota Transplantation involves transmitting the patient from a healthy donor to the patient and has shown the results associated with the treatment of gut conditions. This intervention may also be possible in the context of cardiovascular diseases.