Nutrition and the Brain-Heart Connection

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Abstract:The immediate triggers of acute heart attack or acute coronary syndrome (ACS) are not known exactly. There is a marked increase in sympathetic activity, neuroendocrino-logical dysfunction, oxidative stress and deficiency of 3 fatty acids, vitamins, minerals, as well as antioxidants during ACS. Energy intake and expenditure have diurnal variation throughout 24-hour cycle and any disturbance in this cycle may result into disruption of the endogenous clock and neurohumoral dysfunctions. Clinical studies have reported an increased incidence of reinfarction, sudden death, coronary constriction, myocardial ischaemia, vascular variability disorders and angina, during second quarter of the 24 hour cycle, at the point where there is rapid withdrawal of vagal activity and increase in sympathetic tone. In several studies, among patients with heart attack, there was a significant 2-3 fold increase in cardiac events in the second quarter of the day (6-12 hours) compared to other quarters respectively. Triggers of heart attack were noted in up to 80.0% of patients in various studies. Brain related and psychological mechanisms, i.e., emotional stress, sleep deprivation, cold climate, hot climate, large meals and physical exertion were observed among 30-50% of patients. Such triggers have also been reported in Europe, North America and Asia. These triggering factors are known to enhance sympathetic activity and decrease vagal tone, resulting into increased secretion of plasma cortisol, noradrenaline, aldosterone, angiotensin converting enzyme, interleukin-1, 2, 6, 18 and tumor necrosis factor-alpha, that are proinflammatory. There is also a deficiency in the serum levels of 3 fatty acids, vitamin A, E, C, coenzyme Q10, magnesium, potassium, melatonin, interleukin-10 (antiinflammatory) and increase in TBARS, MDA, diene conjugates, TNF-alpha and IL-6, which are indicators of oxidative damage and inflammation, respectively. It is not clear whether the predisposition of ACS is due to size of the meals or other proinflammatory factors of meals.

Section: The Evolution Of Triggersmentioning

confidence: 97%

Section: The Evolution Of Triggersmentioning

confidence: 99%

Section: The Evolution Of Circadian Rhythmmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Potential Chonobiological Triggering Factors of Acute Heart Attack

Sergey¹,

Rapoport²,

Агарвал³

et al. 2010

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Potential Chonobiological Triggering Factors of Acute Heart Attack~!2009-12-29~!2010-01-11~!2010-04-22~!

Sergey¹,

Rapoport²,

Агарвал³

et al. 2010

Self Cite

The immediate triggers of acute heart attack or acute coronary syndrome (ACS) are not known exactly. There is a marked increase in sympathetic activity, neuroendocrino-logical dysfunction, oxidative stress and deficiency of 3 fatty acids, vitamins, minerals, as well as antioxidants during ACS. Energy intake and expenditure have diurnal variation throughout 24-hour cycle and any disturbance in this cycle may result into disruption of the endogenous clock and neurohumoral dysfunctions. Clinical studies have reported an increased incidence of reinfarction, sudden death, coronary constriction, myocardial ischaemia, vascular variability disorders and angina, during second quarter of the 24 hour cycle, at the point where there is rapid withdrawal of vagal activity and increase in sympathetic tone. In several studies, among patients with heart attack, there was a significant 2-3 fold increase in cardiac events in the second quarter of the day (6-12 hours) compared to other quarters respectively. Triggers of heart attack were noted in up to 80.0% of patients in various studies. Brain related and psychological mechanisms, i.e., emotional stress, sleep deprivation, cold climate, hot climate, large meals and physical exertion were observed among 30-50% of patients. Such triggers have also been reported in Europe, North America and Asia. These triggering factors are known to enhance sympathetic activity and decrease vagal tone, resulting into increased secretion of plasma cortisol, noradrenaline, aldosterone, angiotensin converting enzyme, interleukin-1, 2, 6, 18 and tumor necrosis factor-alpha, that are proinflammatory. There is also a deficiency in the serum levels of 3 fatty acids, vitamin A, E, C, coenzyme Q10, magnesium, potassium, melatonin, interleukin-10 (antiinflammatory) and increase in TBARS, MDA, diene conjugates, TNF-alpha and IL-6, which are indicators of oxidative damage and inflammation, respectively. It is not clear whether the predisposition of ACS is due to size of the meals or other proinflammatory factors of meals.

About the Editor

Singh¹

2011

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Dr. Ram B Singh comes from a multidisciplinary background. He began his career with an undergraduate degree in Science, followed by a Medical Science degree, and an MD degree in Internal Medicine with specialization in Cardiology. Dr. Singh further extended his career specializing in the area of Nutritional Science. During the subsequent years, He became much involved in clinical research, integrating nutrition and cardiovascular disease (CVD) along with its risk factors.Dr. Singh's research, especially on magnesium relating to CVD has received a great deal of international recognition. He was first to (a) perform Radioimmunoassay of serum digoxin in relation to digoxin intoxication in the year 1971-73 [1, 2], (b) demonstrate the role of magnesium deficiency in the pathogenesis of arrhythmias in patients with digoxin toxicity [3], (c) develop a concept of magnesium deficiency as a risk factor of digitalis intoxication [4], (d) report magnesium deficiency among patients with pulmonary heart disease [5] and atrial fibrillation (96), and (e) propose that magnesium deficiency is a risk factor for refractory cardiac arrhythmias [6] as well as for the elderly [7]. Furthermore, Dr Singh was first to report the role of magnesium deficiency in the pathogenesis of digoxin toxicity in children [8] with particular emphasis of its role in coronary artery disease (CAD), sudden cardiac death (SCD) [9,10], and ventricular fibrillation [10]. These reports earned him an invitation by the editor of the American Heart Journal to write an annotation [11] and by the editor of the Practical Cardiology to write a review article [12]. Dr Singh proposed that the role of magnesium deficiency and its repairement in the neurons, cardiomyocytes, , arterial endothelial and smooth muscle cells are important factors in predisposing CAD and SCD [12,13]. He reported the association between chronic active hepatitis and cardiomyopathy [14] and magnesium deficiency in the brain predisposing sudden death and the role of magnesium and potassium in hypertension [15][16][17][18][19]. Dr. Singh proposed a hypothesis that calcium channel antagonists modulate calcium by increasing magnesium influx by influencing magnesium ATPase and magnesium channels [20]. It is known that calcium channel blockers do not block the calcium channels, but they simply delay the opening of the channels, resulting in a decreased entry of calcium.