Essential Mineral Intake for Cardiovascular Disease | Wellness Clinic

An improper diet and nutrition can often lead to a variety of health issues, such as cardiovascular disease and hypertension. Additionally, other food-related risk factors can include, high blood pressure, or BP, obesity and type 2 diabetes. Saturated and trans fats, for example, can increase cholesterol in the blood. It's this build-up of fatty deposits in the coronary arteries, which can lead to cardiovascular disease, hypertension and even heart attacks.

Which vitamins and minerals can improve cardiovascular disease and hypertension?

A healthy balance of vitamins and minerals can help manage and maintain heart health. According to research studies, the right intake of potassium, magnesium, calcium and zinc can substantially improve cardiovascular disease and hypertension. A proper diet and nutrition can have similar effects as taking cardiovascular disease and hypertension drugs and medications, but through a much more natural approach.

Potassium

The average U.S. dietary intake of potassium (K+) is 45 mmol/d with a potassium to sodium (K+/Na+) ratio of less than 1:2. The suggested intake of K+ is 4700 mg/d (120 mmol) with a K+/Na+ ratio of about 4-5 to 1. Several clinical and observational trials have demonstrated a substantial decrease in BP with greater K+ intake in hypertensive patients. The normal blood pressure reduction with a K+ supplementation of 60 to 120 mmol/d is 4.4/2.5 mmHg in hypertensive patients but may be as far as 8/4.1 mmHg with 120 mmol/d (4700 mg). In hypertensive patients, the linear dose response relationship is 1.0 mmHg reduction in systolic blood pressure, or SBP, and 0.52 mmHg decrease in diastolic blood pressure, or DBP, that a 0.6 g/d growth in dietary fiber intake. The solution can involve race (black > white), sodium, magnesium and calcium intake. Those on a higher sodium intake have a greater decrease in BP. Alteration of this K+/Na+ ratio is very important to the two polyunsaturated and outcomes. High potassium intake reduces the prevalence of cardiovascular disease independent of their BP reduction. Furthermore, If the serum potassium is less than 4.0 meq/dL, there is a higher risk of CVD mortality, ventricular tachycardia, and ventricular fibrillation. Red blood cell potassium is a sign of overall body stores and CVD risk in comparison to the serum potassium. Gu et al discovered that potassium supplementation in 60 mmol of KCl Daily for 12 wk significantly reduced SBP -5.0 mmHg (range -2.13 into -7.88 mmHg) (p < 0.001) in 150 Chinese men and women aged 35 to 64 decades.

Insulin raises natriuresis, modulates sensitivity, vasodilates, reduces the sensitivity to catecholamines and Angiotensin II, raises nitric oxide ATPase and DNA synthesis in the vascular smooth muscle cells and decreases sympathetic nervous system activity. In addition, potassium increases bradykinin and prostate kallikrein, decreases NADPH oxidase, which reduces oxidative stress and inflammation, improves insulin sensitivity, reduces ADMA, reduces intracellular sodium and reduces production of TGF-β.Each 1000 mg increase in potassium intake per day reduces all cause mortality by approximately 20 percent. Potassium intake of 4.7 g/d is estimated to decrease CVA by 8 percent to 15 percent and MI by 6 percent to 11 percent. Numerous SNP's, such as nuclear receptor subfamily 3 group C, angiotensin IItype receptor and hydroxysteroid 11 beta dehydrogenase (HSD11B1 and B2) determine an individual's reaction to dietary potassium intake towards their overall health and wellness.

Each 1000 mg drop in sodium intake daily will reduce all cause mortality. A recent study indicated a dose related response to CVA. There has been a RRR of CVA of 23 percent at 1.5-1.99 gram, 27% at 2.0-2.49 g, 29 percent at 2.5-3 g and 32 percent more than 3 g/d of potassium urinary excretion. The recommended daily dietary intake for individuals with hypertension is 4.7 to 5.0 g of potassium and less than 1500 milligrams of sodium. Potassium used out of supplementation should be decreased with care in patients with renal impairment or those ARB, DRI and serum aldosterone receptor antagonists.

Magnesium

A high dietary intake of magnesium of at least 500-1000 mg/d reduces BP in the majority of the reported observational epidemiologic and clinical trials, but the outcomes are much less consistent than those seen with K + and Na +. There's an inverse relationship between BP and dietary magnesium intake. A report on 60 essential hypertensive subjects given magnesium supplements showed a substantial decrease in blood pressure in an eight week interval reported by 24 h ambulatory BP, office and home BP. The maximum decrease in clinical trials has been 5.6/2.8 mmHg but some studies have shown no change in BP. The blend of high potassium and low sodium intake with increased magnesium intake had.

Magnesium also raises the effectiveness of all anti-hypertensive drugs and medications, according to research studies. Magnesium competes with Na+ for binding sites on vascular smooth muscle and also functions as a direct vasodilator, . Magnesium increases prostaglandin E (PGE), modulates intracellular sodium, potassium, calcium and pH, increases nitric oxide, improves adrenal function, reduces oxLDL, reduces HS-CRP, TBxA2, A-II, and norepinephrine. Magnesium also enhances insulin resistance, glucose and MS, binds at a necessary cooperative manner with potassium, causing EDV and BP reduction, reduces CVD and cardiac arrhythmias, reduces carotid IMT, reduces cholesterol, reduces cytokine production, inhibits nuclear factor Kb, reduces oxidative stress and inhibits platelet aggregation to reduce thrombosis. Magnesium is an essential co-factor because of its delta-6-desaturase enzyme that for conversion of linoleic acid (LA) to gamma linolenic acid (GLA) required for synthesis of this vasodilator and platelet inhibitor PGE1.

A meta-analysis of all 241378 patients utilizing 6477 strokes showed a reverse relationship of dietary magnesium to the incidence of stroke. For each 100 milligrams of magnesium intake, stroke diminished. The mechanism comprise inhibition of induced glutamate release, NMDA receptor blockade, CCB actions reduction in vasodilation and ATP depletion of the arteries. A meta-analysis showed discounts mmHg in 22 trials of 1173 patients. Intracellular level of calcium (RBC) is more indicative of overall body shops and should be quantified along with serum and urinary magnesium. Magnesium might be supplemented in doses of 500. Magnesium formulations may improve absorption and reduce the incidence of diarrhea. Adding taurine in 1000 increases the ramifications of magnesium. Magnesium supplements should be avoided or used with caution in individuals with renal insufficiency.

Calcium

Population studies reveal a link between hypertension and calcium, but clinical trials that handled calcium supplements have shown consequences on blood pressure. The heterogeneous responses to calcium supplementation have been clarified through research studies. This is really the "ionic hypothesis" of hypertension, cardiovascular disease and associated cognitive, cognitive and functional disorders. Calcium supplementation is not recommended at this time as an effective method to decrease blood pressure due to insufficient research studies on its use.

Zinc

Low serum zinc levels in observational research and hypertension correlate as well as CHD, type II DM, hyperlipidemia, elevated lipoprotein that a [Lp(a)], increased 2 h post-prandial plasma glucose levels and insulin resistance. Zinc is hauled to vascular and cardiac muscle and cells by metallothionein. Deficiencies of metallothionein with intramuscular zinc deficiencies can lead to cardiomyocyte oxidative stress , mitochondrial dysfunction, dysfunction and apoptosis with cardiac remodeling hypertension, cardiovascular disease, heart failure, or fibrosis. Intracellular calcium increases oxidative.

Bergomi et al assessed Zinc (Zn++) status in 60 hypertensive subjects compared to 60 normotensive control subjects. A reverse correlation of serum Zn++ and BP has been observed. The BP was inversely associated with a Zn++ dependent enzyme lysyl oxidase activity. Zn++ inhibits gene expression and transcription through NF-κBand activated protein-1 and is now a significant co-factor for SOD. These impacts plus those on insulin resistance and SNS consequences, membrane ion exchange, RAAS might account for Zn++ antihypertensive effects. Intake needs to be 50 mg/d.

Individuals with cardiovascular disease and hypertension can benefit from the proper diet and nutrition. Essential vitamins and minerals found in a balanced, healthy nutrition, such as potassium, magnesium, calcium and zing, among others, can help improve heart health. Deficiencies in these and a diet full of saturated and trans fats can increase the prevalence of cardiovascular disease. While diagnosis and drugs/medications can be prescribed to treat cardiovascular disease and hypertension, a balanced diet and nutrition can have similar effects. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please contact the proper healthcare professionals.

By Dr. Alex Jimenez