Hypertension is a progressively damaging disease that affects over 30% of our population over 20 years of age. In a survey done in 2004, the number of physician office visits for high blood pressure was estimated at 38 million. It is a leading cause of cardiovascular disease and stroke.
It has many underlying causes including overweight, magnesium, potassium and calcium deficiency, liver, kidney and heart disease, alcohol overuse, aging, insulin resistance, and stress.
Often it is diagnosed late, where people have it without symptoms. Organ involvement can begin relatively early.
The traditional approach to hypertension usually involves a simple blood pressure reading and then a prescription for medication. In many cases this may be the wrong thing to do.
In my experience, and in medical literature, many people can have elevation of blood pressure from deficiencies of minerals. These include Magnesium, Potassium and Calcium.
We take it for granted that if we eat a "well balanced diet", whatever that is, then we will have enough vitamins and minerals. This is so far from the truth.
In testing many thousands of patients for nutrients I frequently see deficiency.
Many of the first line medications used for Hypertension are diuretics, and these deplete magnesium and potassium. !!!!!
So sometimes the treatment can worsen the cause. In these cases doctors will then use additional medication because the first doesn’t work.
When in reality testing for the nutrients and correcting deficiency will correct the cause of the problem.
Please read the following articles.
Thank You,
Dr. Chris Calapai
Role of magnesium in the pathogenesis of hypertension
Human essential hypertension is a complex, multifactorial, quantitative trait under polygenic control. Although the exact etiology is unknown, the fundamental hemodynamic abnormality in hypertension is increased peripheral resistance, due primarily to changes in vascular structure and function. These changes include arterial wall thickening, abnormal vascular tone and endothelial dysfunction and are due to alterations in the biology of the cellular and non-cellular components of the arterial wall.
Many of these processes are influenced by magnesium. Small changes in magnesium levels may have significant effects on cardiac excitability and on vascular tone, contractility and reactivity. Accordingly magnesium may be important in the physiological regulation of blood pressure whereas perturbations in cellular magnesium homeostasis could play a role in pathophysiological processes underlying blood pressure elevation.
For the most part, epidemiological and experimental studies demonstrate an inverse association between magnesium and blood pressure and support a role for magnesium in the pathogenesis of hypertension. However data from clinical studies have been less convincing and the therapeutic value of magnesium in the prevention and management of essential hypertension remains unclear. In view of the still ill-defined role of magnesium in clinical hypertension, magnesium supplementation is advised in those hypertensive patients who are receiving diuretics, who have resistant or secondary hypertension or who have frank magnesium deficiency.
A magnesium-rich diet should be encouraged in the prevention of hypertension, particularly in predisposed communities because of the other advantages of such a diet in prevention. The clinical aspect that has demonstrated the greatest therapeutic potential for magnesium in hypertension, is in the treatment of pre-eclampsia and eclampsia. The present review discusses the role of magnesium in the regulation of vascular function and blood pressure and the implications in mechanisms underlying hypertension. Alterations in magnesium regulation in experimental and clinical hypertension and the potential antihypertensive therapeutic actions of magnesium will also be addressed.
Role of magnesium in hypertension
Magnesium affects blood pressure by modulating vascular tone and reactivity. It acts as a calcium channel antagonist, it stimulates production of vasodilator prostacyclins and nitric oxide and it alters vascular responses to vasoactive agonists. Magnesium deficiency has been implicated in the pathogenesis of hypertension with epidemiological and experimental studies demonstrating an inverse correlation between blood pressure and serum magnesium levels. Magnesium also influences glucose and insulin homeostasis, and hypomagnesemia is associated with metabolic syndrome. Although most epidemiological and experimental studies support a role for low magnesium in the pathophysiology of hypertension, data from clinical studies have been less convincing. Furthermore, the therapeutic value of magnesium in the management of hypertension is unclear. The present review addresses the role of magnesium in the regulation of vascular function and blood pressure and discusses the implications of magnesium deficiency in experimental and clinical hypertension, in metabolic syndrome and in pre-eclampsia.
Quantitative Study of Circadian Variations of Ambulatory Blood Pressure in Chinese Healthy, Hypertensive, and Diabetes Subjects
Ambulatory blood pressure monitoring (ABPM) recorded abundant data of BP and heart rate (HR) variations with even more derived parameters for evaluation of BP. Using our ABP database system established recently, we studied quantitatively the data of 24-hr ABP in Chinese.
First, 155 Chinese were divided into three groups: 50 healthy subjects (C) of 20 men and 30 women, aged 60.0В В±В 10.3 (SD) years; 58 hypertensive patients (H, mild or moderate hypertension) of 33 men and 25 women, aged 59.4В В±В 8.0 years; 47 diabetes patients (D, type 2 diabetes, all were normotensive and with no insulin treatment) with 28 men and 19 women, aged 61.0В В±В 8.5 years. Then 24-hr ABP was monitored by TM-2421 Monitor and data were analyzed by ABP database, cosinor method, and conventional statistics.
Our results were 4-fold: 1) systolic BP (SBP), diastolic BP (DBP), HR, rate-pressure product (HRВ Г—В SBP) showed circadian variations, and significant circadian rhythms were confirmed by cosinor method in all groups. MESOR (midline estimate statistic of rhythm) differed significantly among three groups (H had the highest and C had the lowest values); 2) BP means (SBP, DBP, pulse pressure [PP], and HRВ Г—В SBP) and BP loads (SBP, DBP, and PP) showed significant differences among the groups (H and D had higher values than that of C); 3) there were no significant differences of BP variability (BPV) of SBP, DBP, and PP among the groups; 4) areas under curve of BP (SBP, DBP, and PP) in H were significantly higher than in C and there was no significant difference between H and D.
We concluded that ABPM can offer abundant information on BP evaluation by its direct recording data and derived parameters. The computerized way of treating the large numbers of ABPM values supplies a useful tool in evaluation of BP. Our results suggest that clinically normotensive diabetes patients had some pathological alterations in their BP systems.
Magnesium Deficiency in Critical Illness
Magnesium (Mg) deficiency commonly occurs in critical illnessand correlates with a higher mortality and worse clinical outcomein the intensive care unit (ICU). Magnesium has been directlyimplicated in hypokalemia, hypocalcemia, tetany, and dysrhythmia.
Moreover, Mg may play a role in acute coronary syndromes, acutecerebral ischemia, and asthma. Magnesium regulates hundredsof enzyme systems. By regulating enzymes controlling intracellularcalcium, Mg affects smooth muscle vasoconstriction, importantto the underlying pathophysiology of several critical illnesses.
The principle causes of Mg deficiency are gastrointestinal andrenal losses; however, the diagnosis is difficult to make becauseof the limitations of serum Mg levels, the most common assessmentof Mg status. Magnesium tolerance testing and ionized Mg2+ arealternative laboratory assessments; however, each has its owndifficulties in the ICU setting.
The use of Mg therapy is supportedby clinical trials in the treatment of symptomatic hypomagnesemiaand preeclampsia and is recommended for torsade de pointes.Magnesium therapy is not supported in the treatment of acutemyocardial infarction and is presently undergoing evaluationfor the treatment of severe asthma exacerbation, for the preventionof postcoronary bypass grafting dysrhythmias, and as a neuroprotectiveagent in acute cerebral ischemia.
Potassium in Hypertension