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Kraków, Poland

Hristova K.,Sofia University | Singh R.B.,Halberg Hospital and Research Institute | Fedacko J.,Safaric University | Toda E.,Tokai University | And 6 more authors.
World Heart Journal | Year: 2013

Introduction. Recent evidence shows that chronic heart failure (CHF) is a major cause of morbidity and mortality. The prognosis in CHF may be dependent on cause, severity and presence of risk factors and drug therapy. In the present study, we examine the causes, risk factors, class and oxidative stress among CHF patients. Subjects and methods. Of 127 patients with CHF, 2 were excluded and the remaining 125 patients (Men 61, women 64) with different aetiologies of CHF, and 250 age and sex matched control subjects, were evaluated in this case study. Severity of disease based on the New York Heart Association (NYHA) standards fell within functional classes II to IV. The diagnosis of HF was based on clinical manifestations as well as on echocardiographic heart enlargement. Results. The causes of CHF were; CAD (n=34, 27.2%), hypertensive heart disease (n=10, 8.0%),valvular heart disease (n=40, 32.0%) and idiopathic dilated cardiomyopathy (n=38, 30.4%).Risk factors of HF were; CAD (n=52, 41.6%), hypertension (>140/90mmHg) (n=54, 43.2%), diabetes mellitus (n=12, 9.6%), obesity (n=43, 34.4%) and albuminurea (n=12,9.6%). Echocardiographic ejection fraction was 39.1±8.2% (mean±SD)in the study group, indicating class II-IV heart failure. There was a significant increase in biomarkers of oxidative stress, among HF patients compared to healthy subjects. Conclusions. The findings indicate that HF has become a public health problem. The causes of HF appear to be CAD, cardiomyopathy and valvular heart disease. Severity of CHF, aetiology; CAD and cardiomyopathy appear to be important for increased oxidative stress among these patients. © Nova Science Publishers, Inc.

Alam S.E.,University of Delhi | Singh R.B.,The TsimTsoum Institute | Gupta S.,The TsimTsoum Institute | Dherange P.,The TsimTsoum Institute | And 4 more authors.
Canadian Journal of Physiology and Pharmacology | Year: 2012

The impact of diet and environmental factors on genes concerned with epigenetic inheritance and the mechanism of evolution has grown significantly beyond the Modern Synthesis period. Epigenetic inheritance is the passing of phenotypic change to subsequent generations in ways that are outside the genetic code of DNA. Recently, polymorphisms of the human Delta-5 (fatty acid desaturase, FADS1) and Delta-6 (FADS2) desaturase genes have been described as being associated with the level of several long-chain n-3 and n-6 polyunsaturated fatty acids (PUFAs) in serum phospholipids. Increased consumption of refined starches and sugar increases the generation of superoxide anion in the tissues and free fatty acids (FFA) in the blood. There is an increased amount and activity of nuclear factor-κB (NF-κB), a transcriptional factor regulating the activity of at least 125 genes, most of which are pro-inflammatory. The consumption of glucose may be associated with an increase in 2 other pro-inflammatory transcription factors: activating protein-1 (AP-1), and early growth response protein-1 (Egr-1). AP-1 regulates the transcription of matrix metallo-proteinases and Egr-1 modulates the transcription of tissue factor and plasminogen activator inhibitor-1. It is possible that a complex set of factors, including nutritional factors, come into play during epigenetic inheritance.

Singh R.B.,The TsimTsoum Institute | Gupta S.,The TsimTsoum Institute | Dherange P.,The TsimTsoum Institute | de Meester F.,The TsimTsoum Institute | And 3 more authors.
Canadian Journal of Physiology and Pharmacology | Year: 2012

Recent research indicates an association between brain dysfunction and the pathogenesis of metabolic syndrome. To investigate this, we created a Medline search (up to December 2011) of articles in PubMed. The results indicated that refined carbohydrates, saturated and total fat, high levels of ω-6 fatty acids, and low levels of ω-3 fatty acids and other long chain polyunsaturated fatty acids (PUFA), all in conjunction with sedentary behaviour and mental stress can predispose to inflammation. Increased sympathetic activity, with increased secretion of catecholamine, cortisol, and serotonin can cause oxidative stress, which may damage the arcuate nucleus as well as the hypothalamus and macrophages, and the liver may release pro-inflammatory cytokines. These, in conjunction with an underlying deficiency in long chain PUFA, may damage the arcuate nucleus as well as neuropeptide-Y and pro-opiomelanocortin neurons and insulin receptors in the brain, especially during fetal life, infancy, and childhood, resulting in their dysfunction. Of the fatty acids in the brain, 30%-50% are long chain PUFA, which are incorporated in the cell membrane phospholipids. Hence, ω-3 fatty acids, which are also known to enhance parasympathetic activity and increase the secretion of anti-inflammatory cytokines interleukin (IL)-4 and IL-10 as well as acetylcholine in the hippocampus, may be protective. Therefore, treatment with ω-3 fatty acids may be applied for the prevention of metabolic syndrome.

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