Sodium: Cardiovascular disease and hypertension can often occur due to a variety of factors, however, an improper diet and nutrition has been appointed to be one of the most prevalent causes behind the onset of cardiovascular disease and hypertension. While an improper diet and nutrition can lead to these issues, a balanced, healthy diet and nutrition can help prevent cardiovascular disease and hypertension, even treat the existing conditions.
What’s the best dietary and nutritional approach to treat cardiovascular disease and hypertension?
Many of the substances in food, particularly in nutraceutical supplements, antioxidants, vitamins or nutritional supplements, function in a manner that is similar to a category of drugs and medications to improve cardiovascular disease and hypertension. The effect is synergistic when used in combination with other nutritional supplements even though the drug might not be less than the potency of the compounds. These natural compounds have been outlined to the significant antihypertensive drug classes, such as diuretics, beta blockers, central alpha agonists, direct vasodilators, calcium channel blockers (CCB’s), angiotensin converting enzyme inhibitors (ACEI’s), angiotensin receptor blockers (ARB’s) and direct renin inhibitors (DRI).
Dietary Approaches to Stop Hypertension
The Dietary Approaches to Stop Hypertension (DASH) Iand II diets conclusively demonstrated significant reductions in BP in borderline and stageIhypertensive patients. Back in DASH I, untreated hypertensive subjects with SBP < 160 mmHg and DBP 80-95 mmHg were placed on one of three diets for 4 weeks, controled diet, vegetable and fruit diet (F + V) and combined diet, which added F + V and low fat milk. Sodium restriction was added by DASH II in every group. The control diet consisted of sodium at 3 g/d, potassium, calcium and magnesium in 25% of the US average, macronutrients at US average of 4 portions every day, a sodium/potassium ratio of 1.7 and fiber at 9 g/d. The F + V diet raised the potassium, calcium and magnesium to 75 percent, macronutrients compared to the US average, a sodium potassium ratio of 0.7, 31 gram of fiber and 8.5 portions of vegetables and fruits per day. The joint diet was similar to the F + V diet but additional fat milk. At 2 wk the BP was decreased by 10.7/5.2 mmHg from the hypertensive patients in DASHIand 11.5/6.8 mmHg from the hypertensive patients in DASH II. These reductions persisted provided that the patients were on the diet. The DASH diet increases plasma renin activity (PRA) and serum aldosterone levels in response to this BP reductions) The increase in PRA was 37 ng/mL every day. There has been an associated of reaction with the polymorphism of beta 2 adrenergic receptor. The A allele of G46A had blunted PRA and a higher BP reduction and aldosterone. The arachidonic acid (AA) genotype had the best response along with the GG genotype had no response. Adding an ARB, DRI or ACEI improved BP reaction due to blockade of the increase in PRA to the DASH diet at the GG group. A very low sodium DASH diet reduces oxidative stress (urine F2-isoprostanes), enhances vascular function (enhancement indicator) and lowers BP in salt sensitive areas. In addition, plasma nitrite increased and pulse wave velocity decreased on the DASH diet at week two.
Sodium (Na+) Loss and Hypertension
The average sodium intake in the US is 5000 mg/d with some regions of the nation consuming 15000-20000 mg/d. On the other hand, the minimal requirement for sodium is most likely roughly 500 mg/d. Epidemiologic, observational and controlled clinical trials reveal that an increased sodium intake is associated with increased risk for proteinuria, renal insufficiency, CVD LVH, CHD, MI and of the SNS as well as BP. A decrease in sodium intake in hypertensive patients the salt sensitive patients, will significantly lower BP by 4-6/2-3 mmHg that’s proportional to the level of sodium restriction and might stop or delay hypertension in high risk patients and decrease CV events.
Salt sensitivity (≥ 10% increase in MAP with salt loading) occurs in about 51 percent of hypertensive patients and is a vital variable in determining the cardiovascular, cerebrovascular, renal and BP responses to dietary salt intake. Cardiovascular events are prevalent in the salt patients than ones, independent of BP. An increased sodium intake has a direct positive correlation with BP and the risk of CHD and CVA. The risk is independent of BP to get CVA with a relative risk of 1.04 to 1.25 in the lowest to the highest quartile. In addition, patients may convert into a BP routine with increases in nocturnal BP as the sodium intake increases.
Increased sodium intake has a direct impact on endothelial cells. Sodium promotes cutaneous lymphangiogenesis, increases endothelial cell stiffness, reduces dimensions, surface area, volume, cytoskeleton, deformability and pliability, reduces eNOS and NO generation, raises asymmetric dimethyl arginine (ADMA), oxidative stress and TGF-β. Every one of these vascular responses are increased in the presence of aldosterone. These modifications occur independent of BP and may be partially counteract by potassium. The endothelial cells act as vascular salt sensors. Endothelial cells are targets for aldosterone which activate epithelial sodium channels (ENaCs) and also have a negative effects on discharge of NO and on endothelial function. The mechanical stimulation of the cell plasma membrane along with the submembranous actin network (endothelial glcyocalyx) (“shell”) serve as a “firewall” to protect the endothelial cells and are regulated by serum sodium, potassium and aldosterone within the physiological selection. Changes in shear-stress-dependent activity of the endothelial NO synthase located in the caveolae regulate the viscosity in this “shell”. High plasma sodium gelates the casing of the cell, whereas the casing is fluidized by high fructose. These communications between intracellular enzymes and extracellular ions happen in the plasma membrane barrier, whereas 90 percent of the cell mass remains uninvolved in such changes. Blockade of the ENaC using spironolactone (100%) or amiloride (84%) minimizes or prevent many of these vascular endothelial responses and boost NO. Nitric oxide release follows not vice versa and nanomechanics and decreases vascular endothelial cell stiffness which enhances circulation conducive vasodilation that is dependent. In the presence of HS-CRP that was increased and vascular inflammation, the effects of aldosterone on the ENaC is enhanced further raising vascular stiffness and BP. High sodium intake also abolishes the AT2R-mediated vasodilation immediately with complete abolition of endothelial vasodilation (EDV) within 30 d. Thus, it is now clear that high dietary sodium has adverse effects on the circulatory system, BP and CVD by changing the endothelial glycocalyx, which is a negatively charged biopolymer that lines the blood vessels and also serves as a protective barrier against sodium over-load, increased sodium permeability and sodium-induced TOD. Certain SNP’s of salt inducible kinaseIwhich alter Na+/K+ ATPase, determine LVH and sodium caused hypertension.
The sodium intake every day in patients must be between 1500. BP reduction improves in people on patients which are on treatment and the decrease in BP is additive with limitation of refined carbohydrates. Reducing sodium consumption may reduce damage to the brain, heart, kidney and vasculature through mechanisms dependent on the BP reduction that is little as well as those independent of the BP. A balance of sodium with nutrients, particularly calcium, magnesium and potassium is important, not just in reducing and controlling BP, but also in decreasing cerebrovascular and cardiovascular events. An increase in the sodium to potassium ratio is associated with risk of all-cause mortality and CVD. The Yanomamo Indians consume and excrete only 1 meq of sodium from 24 h and consume and excrete 152 meq of potassium in 24 h. BP doesn’t rise with age and is related to elevated PRA, although the Na + to K + percentage is 1/152. Currently 50 the BP in the Yanomamo is 100-108/64-69 mmHg.
In conclusion, Cardiovascular disease and hypertension can often occur due to a variety of factors, however, an improper diet and nutrition has been appointed to be one of the most prevalent causes behind the onset of cardiovascular disease and hypertension. According to the above research studies, an imbalance in the intake of sodium can lead to cardiovascular disease and hypertension. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
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