The Seven Countries Study showed that traditional Japanese and Mediterranean diets are protective against cardiovascular diseases (CVDs). The Japanese diet is considered the healthiest because it provides Japanese populations with the highest longevity and health. DASH and Mediterranean-style diets are also considered healthy diets, although the Indo-Mediterranean-style diet may provide better protective effects among patients with CVDs compared to other diets. The concept of the Indo-Mediterranean type of diet was developed after examining its role in the prevention of CVDs in India, the value of which was confirmed by a landmark study from France: the Lyon Heart Study. These workers found that consuming an alpha-linolenic acid-rich Mediterranean-style diet can cause a significant decline in CVDs and all-cause mortality. Later in 2018, the PREDIMED study from Spain also reported that a modified Mediterranean-style diet can cause a significant decline in CVDs, type 2 diabetes mellitus (T2DM), and cancer. The Indo-Mediterranean diet may be superior to DASH and Mediterranean diets because it contains millets, porridge, and beans, as well as spices such as turmeric, cumin, fenugreek, and coriander, which may have better anti-inflammatory and cardioprotective effects. These foods are rich sources of nutrients, flavonoids, calcium, and iron, as well as proteins, which are useful in the prevention of under- and overnutrition and related diseases. It is known that DASH and Mediterranean-style diets have a similar influence on CVDs. However, the Indo-Mediterranean-style diet may be as good as the Japanese diet due to improved food diversity and the high content of antioxidants.
The exact pathophysiology of heart failure (HF) is not yet known. Western diet, characterized by highly sweetened foods, as well as being rich in fat, fried foods, red meat and processed meat, eggs, and sweet beverages, may cause inflammation, leading to oxidative dysfunction in the cardiac ultra-structure. Oxidative function of the myocardium and how oxidative dysfunction causes physio-pathological remodeling, leading to HF, is not well known. Antioxidants, such as polyphenolics and flavonoids, omega-3 fatty acids, and other micronutrients that are rich in Indo-Mediterranean-type diets, could be protective in sustaining the oxidative functions of the heart. The cardiomyocytes use glucose and fatty acids for the physiological functions depending upon the metabolic requirements of the heart. Apart from toxicity due to glucose, lipotoxicity also adversely affects the cardiomyocytes, which worsen in the presence of deficiency of endogenous antioxidants and deficiency of exogenous antioxidant nutrients in the diet. The high-sugar-and-high-fat-induced production of ceramide, advanced glycation end products (AGE) and triamino-methyl-N-oxide (TMAO) can predispose individuals to oxidative dysfunction and Ca-overloading. The alteration in the biology may start with normal cardiac cell remodeling to biological remodeling due to inflammation. An increase in the fat content of a diet in combination with inducible nitric oxide synthase (NOSi) via N-arginine methyl ester has been found to preserve the ejection fraction in HF. It is proposed that a greater intake of high exogenous antioxidant restorative treatment (HEART) diet, polyphenolics and flavonoids, as well as cessation of red meat intake and egg, can cause improvement in the oxidative function of the heart, by inhibiting oxidative damage to lipids, proteins and DNA in the cell, resulting in beneficial effects in the early stage of the Six Stages of HF. There is an unmet need to conduct cohort studies and randomized, controlled studies to demonstrate the role of the HEART diet in the treatment of HF.
Chronic heart failure (CHF) has different stages and includes pre‐HF (PHF), a state of high risk of developing myocardial dysfunction and advanced CHF. Some major behavioral risk factors of PHF might predispose to biological risk factors such as obesity, diabetes mellitus, dyslipidemia, hypertension, myocardial infarction, and cardiomyopathy. These risk factors damage the myocytes leading to fibrosis, apoptosis, cardiac hypertrophy, along with alterations in cardiomyocyte’ size and shape. A condition of physiological subcellular remodeling resulting into a pathological state might be developed, conducting to PHF. Both PHF and heart failure (HF) are associated with the activation of phospholipases and protease, mitochondrial dysfunction, oxidative stress and development of intra‐cellular free Ca2+ [Ca2+]i overloading to an elevation in diastolic [Ca2+]i. Simultaneously, cardiac gene expression is activated leading to further molecular, structural and biochemical changes of the myocardium. The sub‐cellular remodeling may be intimately involved in the transition of cardiac hypertrophy to heart failure. 2D‐ and 3D‐speckle tracking echocardiography (STE) have been used to quantify regional alterations of longitudinal strain and area strain, through their polar projection, which permits a further assessment of both sites and degrees of myocardial damage. The examination of strain can identify sub‐clinical cardiac dysfunction or cardiomyocyte remodeling. During remodeling of the myocardium cardiac strain is attenuated, therefore it is an indicator of disease assessment.
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