Search

Sudden cardiac death (SCD) is a sudden unexpected death due to a demise of the myocardium. SCD also includes an acute precipitating trigger that lies in the brain and a chronic electrical instability of the myocardium. Most SCDs in absolute terms occur in subjects with no known pre-existing heart disease. The incidence of SCD may be about 20% per year in patients with heart failure and those with markers of arrhythmias, compared with about 1-2% in the general population, i.e., subjects with no “known” pre-existing heart disease. Some early symptoms of SCD include fatigue, fainting, blackouts and dizziness due to blood stopping to flow to the brain and other organs of the body. SCD is responsible for a sizable portion of the over 19 million deaths globally each year from CVDs. Acute anxiety, hypertension, hyperlipidemia, family history, arrhythmias, diabetes mellitus, prediabetes, metabolic syndrome and obesity are risk factors to precipitate SCD. In addition, other behavioral risk factors including type A personality, physical inactivity, smoking, male gender, women after menopause, unhealthy diet and modern lifestyle, such as regularly eating fast foods or foods rich in saturated fats, and late-night sleep; excess sugar, alcohol and salt intake can also predispose to SCD. Deficiency in some cations and vitamins, especially magnesium, potassium, flavonoids and trace elements, and thiamine, have been associated with SCD. One or a combination of these risk factors can lead to pathological conditions and cardiovascular diseases (CVDs) that predispose to SCD. The most common physio-pathological event is the rupture of the vulnerable atherosclerotic plaque with athero-thrombosis, observed in the majority of the patients with acute coronary syndromes (ACSs) and SCD. In an animal experiment, it has been reported that neutrophil-depleted animals had worsened cardiac function, increased fibrosis, and progressively developed heart failure, indicating that high neutrophil coun

Modern approaches: moderate physical activity, a functional food-rich diet, reduction of body weight, control of blood pressure and blood lipids by drug therapy, cessation of tobacco and alcohol use, for health promotion and prevention of non-communicable diseases (NCDs) have only partial benefit on future risk of these diseases, despite the high health budget in high-income countries. Holistic approaches to health education and holistic health may provide better health and may be more successful in the prevention of cardiovascular diseases (CVDs) and other chronic diseases. There is evidence that psychosocial stress, late night sleep and late night eating, as well as sleep deprivation, deficiency of nutrients such as omega-3 fatty acids, vitamins and flavonoids can have adverse effects on brain-body mechanisms, resulting in obesity and insulin resistance, leading to CVDs and other chronic diseases. However, active prayer, kirtan krea, verbalization, yogasan and meditation, along with Mediterranean style-functional food-rich diet as well as nutraceuticals and herbs may be protective against NCDs. © 2017 Nova Science Publishers, Inc.

Apart from the sympathetic and parasympathetic nerves, the pituitary and pineal glands and the suprachiasmatic nucleus are also involved in determining autonomic functions. Western diet, autonomic dysfunction and obesity are further associated with sympathetic activation that promotes atherosclerosis, end-organ damage, and hypertension. Experimental sites indicate that high-fatinduced weight gain in rats elevates plasma leptin at 1 to 3 days after the onset of calorie-dense diets, and that dietinduced overfeeding may increase sympathetic activity within 1 week after the onset of the regimen. It has been shown, for the first time, that the high-fat, cafeteria-style diet stimulates sustained increases in lumbar sympathetic neural drive in rats. Halberg demonstrated for the first time in 1973 that eating dinner was associated with relative weight gain, whereas eating the same amount of calories as breakfast was linked to relative weight loss in humans and death in animals. There appear to be independently variable effects on circadian physiology and metabolism in association with circadian restriction of feeding to a particular time of the day and during caloric restriction. Apart from these markers related to energy, circadian alteration in metabolism of nutrients, omega-3 fatty acids, flavonoids, B vitamins and coenzyme Q10 may be important in autonomic functions. © 2015 Nova Science Publishers, Inc.

Background. Brain-derived neurotrophic factor (BDNF), a major neurotrophin, and vascular endothelial growth factor (VEGF) have a documented role in neurogenesis, angiogenesis, and neuronal survival. BDNF can benefit infarct size and functional motor recovery after an ischemic brain lesion in stroke. BDNF also appears to be involved in the pathogenesis of several cardiometabolic disorders, indicating that it is important in brain-body dysfunctions. This review examines the available evidence about the role of BDNF in the development of cardiometabolic vascular risk. Methods. Internet search and discussion with peer colleagues. Results. Several studies have demonstrated that phenotypes associated with insulin resistance are at increased risk for developing cognitive decline and neurodegeneration, vascular dementia, depression and diabetes mellitus and metabolic syndrome which are risk factors for CVDs. BDNF is a member of the neurotrophin family, which interacts with high affinity with tyrosine receptor kinase B and is abundantly expressed in central and peripheral nervous system and can cross the blood-brain barrier in both directions. Majority of the BDNF (70-80%) is derived from brain but it is also present in other body tissue. Apart from lipid and glucose metabolism, BDNF also controls the food intake and appetite. Lower serum BDNF and higher VEGF concentrations were associated with increased risk of incident stroke/TIA. BDNF and VEGF seem to be novel risk markers and may improve stratification of patients at risk for stroke/TIA. Increased concentrations of BDNF were also associated with less white matter hyperintensity and better visual memory. BDNF may serve as an intermediate biomarker for subclinical vascular disease. It may have biological potential to serve as a therapeutic target for primary and secondary prevention of cardiometabolic risk as well as clinical and subclinical vascular brain disease. BDNF deficiency has been observed in association with depr

[No abstract available]

Apart from the sympathetic and parasympathetic nerves, the pituitary and pineal glands and the suprachiasmatic nucleus are also involved in determining autonomic functions. Western diet, autonomic dysfunction and obesity are further associated with sympathetic activation that promotes atherosclerosis, end-organ damage, and hypertension. Experimental sites indicate that high-fat-induced weight gain in rats elevates plasma leptin at 1 to 3 days after the onset of calorie-dense diets, and that dietinduced overfeeding may increase sympathetic activity within 1 week after the onset of the regimen. It has been shown, for the first time, that the high-fat, cafeteria-style diet stimulates sustained increases in lumbar sympathetic neural drive in rats. Halberg demonstrated for the first time in 1973 that eating dinner was associated with relative weight gain, whereas eating the same amount of calories as breakfast was linked to relative weight loss in humans and death in animals. There appear to be independently variable effects on circadian physiology and metabolism in association with circadian restriction of feeding to a particular time of the day and during caloric restriction. Apart from these markers related to energy, circadian alteration in metabolism of nutrients, omega-3 fatty acids, flavonoids, B vitamins and coenzyme Q10 may be important in autonomic functions. © 2016 Nova Science Publishers, Inc.

[No abstract available]

Background: Cardiometabolic risk has been reported to be significantly high among South Asian immigrants to developed countries, compared to people living in South Asian countries. This may be due to disruption of metabolic cycles. Halberg proposed that restricted feeding at a particular time of the day and low calorie intake have independent effects on body weight. This study examines the association of circadian restricted feeding in conjunction with low calorie diet in patients with risk of CVDs and type 2 diabetes mellitus. Subjects and Methods: This study included 32 volunteers, 25-67 years of age, receiving low caloric diet with circadian restricted feeding. All volunteers had an available medical record of overweight (n = 2), obesity (n = 5), hypertension (n = 12), type 2 diabetes mellitus (n = 9) or angina pectoris (n = 4). We randomly selected age- and gender-matched urban patients (n = 500) with known type 2 diabetes and/or hypertension and/or coronary artery disease (CAD) for comparison with volunteers on low caloric diets. Multivariate logistic regression analysis was applied to seek associations of protective or risk factors relative to CVDs and type 2 diabetes. Results: Mean body weight, body mass index, and systolic and diastolic blood pressure were significantly lower in the study group, compared to high-risk urban participants. Fasting blood glucose, triglycerides and total cholesterol, and HDL cholesterol were significantly lower in the study group, compared to high-risk urban subjects. Multivariate logistic regression analysis after adjustment of age and body mass index revealed that the relative risk (RR) and confidence interval of difference (CI) for restricted feeding (male: 0.63 [0.59-0.68], P < 0.001; female: 0.65 [0.62-0.69], P < 0.001) and low-calorie intake (male: 0.64 [0.61-0.67], P < 0.001); female: 0.66 [0.63-0.69], P < 0.001) were inversely associated with the risk of CVDs and type 2 diabetes. Total energy intake (male: 0.67 [0.61-0.74

Background. Brain-derived neuro-trophic factor (BDNF), a major neurotrophin, and vascular endothelial growth factor (VEGF) have a documented role in neurogenesis, angiogenesis, and neuronal survival. BDNF can benefit infarct size and functional motor recovery after an ischemic brain lesion in stroke. BDNF also appears to be involved in the pathogenesis of several cardiometabolic disorders, indicating that it is important in brain-body dysfunctions. This review examines the available evidence about the role of BDNF in the development of cardiometabolic vascular risk. Methods. Internet search and discussion with peer colleagues. Results. Several studies have demonstrated that phenotypes associated with insulin resistance are at increased risk for developing cognitive decline and neurodegeneration, vascular dementia, depression and diabetes mellitus and metabolic syndrome which are risk factors for CVDs. BDNF is a member of the neurotrophin family, which interacts with high affinity with tyrosine receptor kinase B and is abundantly expressed in central and peripheral nervous system and can cross the blood-brain barrier in both directions. Majority of the BDNF (70-80%) is derived from brain but it is also present in other body tissue. Apart from lipid and glucose metabolism, BDNF also controls the food intake and appetite. Lower serum BDNF and higher VEGF concentrations were associated with increased risk of incident stroke/TIA. BDNF and VEGF seem to be novel risk markers and may improve stratification of patients at risk for stroke/TIA. Increased concentrations of BDNF were also associated with less white matter hyperintensity and better visual memory. BDNF may serve as an intermediate biomarker for subclinical vascular disease. It may have biological potential to serve as a therapeutic target for primary and secondary prevention of cardiometabolic risk as well as clinical and subclinical vascular brain disease. BDNF deficiency has been observed in association with dep