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      Coping with stress using magnesium

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          Abstract

          Abstract. According to Selye (1907 – 1982) stress is defined as “nonspecific response of the body to any demand”, eliciting the General Adaptation Syndrome, which is characterized by three stages: alarm reaction – adaptation – exhaustion. Hence, a given stressor, e.g., forced muscular work, can be harmful on acute or prolonged exposure (“distress”) or beneficial at increased level of resistance (“eustress”). Magnesium (Mg) acts as physiological Ca 2+ and NMDA receptor antagonist, stimulates GABA A receptors, inhibits glutamate release from presynaptic neurons, and leads to synaptic strengthening. In cats with chronically implanted electrodes, oral Mg caused electrophysiological alterations characteristic for tranquillizing effects. Accordingly, plentiful Mg supply attenuates the release of stress hormones in humans and protects livestock against diverse stressors. Positive effects on mood, sleep, depression, and affective disorders have also been reported. On the other hand, Mg deficiency sensitizes against various stressors, e.g., noise stress, cardiovascular diseases, functional disorders in children and adults, and ethanol withdrawal. Mg deficiency also plays a key pathogenic role in the development of diabetes, hypertension, and osteoporosis. Consequently, plentiful Mg supply is recommended for coping with distress either utilizing its pharmacological or its (patho-)physiological effects.


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          Magnesium: nature's physiologic calcium blocker.

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            Ketamine, magnesium and major depression--from pharmacology to pathophysiology and back.

            The glutamatergic mechanism of antidepressant treatments is now in the center of research to overcome the limitations of monoamine-based approaches. There are several unresolved issues. For the action of the model compound, ketamine, NMDA-receptor block, AMPA-receptor activation and BDNF release appear to be involved in a mechanism, which leads to synaptic sprouting and strengthened synaptic connections. The link to the pathophysiology of depression is not clear. An overlooked connection is the role of magnesium, which acts as physiological NMDA-receptor antagonist: 1. There is overlap between the actions of ketamine with that of high doses of magnesium in animal models, finally leading to synaptic sprouting. 2. Magnesium and ketamine lead to synaptic strengthening, as measured by an increase in slow wave sleep in humans. 3. Pathophysiological mechanisms, which have been identified as risk factors for depression, lead to a reduction of (intracellular) magnesium. These are neuroendocrine changes (increased cortisol and aldosterone) and diabetes mellitus as well as Mg(2+) deficiency. 4. Patients with therapy refractory depression appear to have lower CNS Mg(2+) levels in comparison to health controls. 5. Experimental Mg(2+) depletion leads to depression- and anxiety like behavior in animal models. 6. Ketamine, directly or indirectly via non-NMDA glutamate receptor activation, acts to increase brain Mg(2+) levels. Similar effects have been observed with other classes of antidepressants. 7. Depressed patients with low Mg(2+) levels tend to be therapy refractory. Accordingly, administration of Mg(2+) either alone or in combination with standard antidepressants acts synergistically on depression like behavior in animal models.
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              Issues in contemporary cardiac rehabilitation: a historical perspective.

              Cardiac rehabilitation consists of exercise, psychosocial support and education and is prescribed most often for patients with coronary heart disease. Its purpose is to facilitate readaptation to normal life through the achievement of maximal functional capability and to reduce heart disease risk factors. It began historically with progressive ambulation after myocardial infarction and by 1980 became a standardized inpatient therapy performed according to a stepped procedure. Predischarge exercise testing was added and has become a meaningful contribution to the concept of risk stratification after an acute coronary event. Rehabilitation has subsequently become part of the outpatient environment and is delivered by multiple models. Meta-analyses have shown that rehabilitation reduces overall and cardiovascular deaths by about 20% and sudden death by about 37% during the year after an acute myocardial infarction. The significance of this, however, must now be modulated by the dynamic role of aggressive coronary intervention. Selection for such intervention has become an important adjunctive aspect of rehabilitation. Newer findings suggest that those stratified at low risk will benefit most by the modification of coronary risk factors, and that patients previously thought to be poor candidates for rehabilitation (such as those with significant left ventricular dysfunction and low work capacity) may experience substantial relative functional benefit. Beyond risk stratification, important contemporary issues include surveillance of patients after angioplasty, the effectiveness of rehabilitation in the attenuation or reversal of both native and vein graft atherosclerosis and consideration of such currently emphasized end points as quality of life and economic evaluation.
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                Author and article information

                Journal
                Trace Elements and Electrolytes
                TE
                Dustri-Verlag Dr. Karl Feistle
                0946-2104
                August 27 2018
                Article
                10.5414/TEX01544
                a5975843-31d5-481a-b057-5f1e5448b72b
                © 2018
                History

                Endocrinology & Diabetes,General medicine,Medicine,Gastroenterology & Hepatology,Nutrition & Dietetics
                magnesium,stress,pharmacological and (patho-)physiological effects

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