Heart Health. The heart beats about 2.5 billion times over an individual’s lifetime, pushing millions of gallons of blood to every part of the body. This steady flow carries oxygen, fuel, hormones, other compounds, and essential cells. It also takes away the waste products of metabolism. However, when the heart stops, the essential functions fail.
Given the heart’s never-ending workload, it can also fail. It can be brought down by a poor diet, lack of exercise, smoking, infection, unfortunate genes, and more. One of the key problems is atherosclerosis. This is the accumulation of cholesterol-rich plaque inside the arteries. This plaque can limit blood flow through the arteries, coronary arteries, and other arteries throughout the body. When a plaque breaks apart, it can cause a heart attack or stroke.
Although many develop some form of cardiovascular disease (diseases affecting the heart and blood vessels) as they get older, a healthy lifestyle, especially when starting early, goes a long way to prevent cardiovascular disease. In addition, lifestyle changes and medications can help heart-harming illnesses, like high blood pressure or high cholesterol, before they cause damage. And there are medications, operations, and devices that can help support heart health if damage occurs.
The American Heart Association, or the AHA, has had a consistent, long-standing focus towards providing the public with the necessary information regarding the role of nutrition reducing the risk of cardiovascular disease. Periodic AHA Dietary Guidelines�support a dietary pattern that promotes the consumption of fruits, vegetables, whole grains, low-fat or nonfat dairy products, fish, legumes, poultry, and lean meats. An improper nutrition consisting of foods rich in saturated and trans fats, can raise the human body’s “bad” cholesterol levels, increasing the risk of cardiovascular disease.
How can vitamins improve the risk of cardiovascular disease?
The American Heart Association’s Dietary Guidelines can help with weight control as well as provide a high nutrient density to meet all nutritional needs.�As reviewed in the first AHA Science Advisory, epidemiological and population studies reported that some vitamins, such as vitamin C, vitamin E, vitamin D and vitamin B6 (pyridoxine), may beneficially affect cardiovascular disease. Reducing the overall risk of cardiovascular disease�can be achieved by the long-term consumption of dietary patterns consistent with the AHA Dietary Guidelines. Vitamin C, vitamin E, vitamin D and vitamin B6 (pyridoxine), each perform a specific function in the prevention and improvement of CVD. The following are described in detail, below.
Vitamin C
Vitamin C is a powerful water-soluble electron-donor. At physiologic levels, it is an antioxidant, although at supra-physiologic doses such as those achieved with intravenous vitamin C, it donates electrons to different enzymes in a pro-oxidative effect. At physiologic doses, vitamin C recycles vitamin E, improves ED and produces a diuresis. Intake of vitamin C and plasma ascorbate concentration in humans is related to heart rate, DBP and SBP.
A review of clinical trials suggest that vitamin C dosing in 250 mg twice daily will lower SBP 5-7 mmHg and diastolic BP 2-4 mmHg in more than 8 weeks. Vitamin C may give rise to a sodium water diuresis, enhance nitric oxide, improve endothelial function, increase nitric oxide and PGI2, decrease adrenal hormone production, improve sympathovagal balance, boost RBC Na/K ATPase, boost SOD, improve aortic elasticity and elasticity, enhance circulation conducive vaso-dilation, reduce pulse wave speed and augmentation index, raise cyclic GMP, trigger potassium channels, reduce cytosolic calcium and reduce serum aldehydes. Vitamin C prevents ED, decreasing the binding affinity of the AT 1 receptor for angiotensin II by disrupting the disulfide bridges, it enriches the antihypertensive effects of drugs and medications in the elderly with hypertension. In patients with hypertension already on maximum pharmacologic therapy, 600 mg of vitamin C lowered the BP in 20/16 mmHg. The lower the first ascorbate serum amount, the greater the blood pressure response. A serum level of 100 ?mol/L is recommended. The SBP and 24 ABM reveal the most important reductions with chronic oral administration of Vitamin C. Block et al within an elegant depletion-repletion study of vitamin C revealed an inverse correlation of plasma ascorbate levels, SBP and DBP. At a meta-analysis of thirteen clinical trials jointly with 284 patients, vitamin C in 500 mg/d in more than 6 weeks decreased SBP 3.9 mmHg and DBP 2.1 mmHg. Hypertensive individuals were found to have significantly lower plasma ascorbate levels in comparison with normotensive subjects (40 ?mol/L vs 57 ?mol/L respectively), and plasma ascorbate is inversely correlated with BP even in healthy, normotensive individuals.
Vitamin E
Most studies have not shown reductions in BP with most forms of tocopherols or tocotrienols.. Patients with T2DM and controlled hypertension (130/76 mmHg) on prescription drugs and medications with an average blood pressure of 136/76 mmHg were administered mixed tocopherols containing 60 percent gamma, 25 per cent delta and 15 percent alpha tocopherols. The BP really increased by 6.8/3.6 mmHg in the research patients (de < 0.0001) but was significantly less compared to this growth with alpha tocopherol of 7/5.3 mmHg (p< 0.0001). This might be a reflection of drug interactions with tocopherols via cytochrome P 450 (3A4 and 4F2) and reduction in the serum levels of the pharmacologic therapy treatments that were concurrently being granted to the patients. Gamma tocopherol could have natriuretic effects by inhibition of this potassium channel in the thick ascending limb of the loop of Henle and reduced BP. Insulin sensitivity improves and enhances adiponectin expression through gamma dependent procedures, which have the potential to serum glucose and lower BP. When vitamin E has an effect, it is most likely small and might be restricted to those with cardiovascular disease or untreated hypertensive patients or psychiatric problems, such as hyperlipidemia or diabetes.
Vitamin D
Vitamin D3 may have an independent and immediate role in the regulation of insulin metabolism and BP. Blood pressure, with its consequences, affects the RAA system, control of adrenal glands, immune system, calcium-phosphate metabolism and ED. The circulating PRA amounts are higher which increases angiotensin II if the vitamin D degree is below 30 ng/mL, increases BP and blunts plasma renal blood flow. The lower the degree of vitamin D, the greater the chance of hypertension, with the lowest quartile of serum Vitamin D with an incidence of hypertension in addition to the maximum quartile. Vitamin D3 markedly suppresses renin transcription. Its function in quantity, electrolytes and BP homeostasis indicates that Vitamin D3 is important in amelioration of hypertension. Vitamin D lowers ADMA, suppresses pro-inflammatory cytokines for example TNF-?, raises nitric oxide, improves endothelial function and arterial elasticity, decreases vascular smooth muscle hypertrophy, modulates electrolytes and blood glucose, increases insulin sensitivity, reduces free fatty acid concentration, regulates the expression of the natriuretic peptide receptor additionally reduces HS-CRP.
The hypotensive effect of vitamin D has been inversely related to the pretreatment serum levels of 1,25(OH)2D3and additive to antihypertensive drugs and medications. Pfeifer et al revealed that supplementation with vitamin D3 and calcium is more effective in reducing SBP. In a study, 148 women with low 25(OH)2D3 levels, the management of 1200 mg calcium and 800 IU of vitamin D3 decreased SBP 9.3 percent more (p< 0.02) in comparison to 1200 mg of calcium alone. The HR fell 5.4 percent (p = 0.02), but DBP wasn’t changed. The scope in BP reduction was 3.6/3.1 to 13.1/7.2 mmHg. The reduction in BP is about serum level of vitamin D3, the dose of vitamin D3 and the level of vitamin D3, but BP is reduced only in patients. Although vitamin D deficiency is associated with hypertension in observational studies, their meta-analysis and randomized clinical trials have yielded inconclusive results. Vitamin D receptor gene polymorphisms may effect the risk of hypertension. A 25 hydroxyvitamin D level of 60 ng/mL is suggested.
Vitamin B6 (Pyridoxine)
Low serum vitamin B6 (pyridoxine) levels are linked to hypertension in several individuals. One research study conducted by Aybak et al demonstrated that blood pressure was significantly reduced by high dose vitamin B6 at 5 mg/kg daily for 4 wk by 14/10 mmHg. Pyridoxine (vitamin B6) is a cofactor in neurotransmitter and hormone synthesis in the central nervous system(norepinephrine, epinephrine, serotonin, GABA and kynurenine), raises cysteine synthesis to neutralize aldehydes, improves the production of glutathione, blocks calcium channels, enhances insulin resistance, reduces central sympathetic tone and reduces end organ responsiveness to glucocorticoids and mineralo-corticoids. Vitamin B6 is decreased using pyrollactams and chronic therapy. Vitamin B6 has actions to diuretics alpha agonists and CCB’s. The proposed dose is 200 mg/d orally.
In conclusion, individuals with cardiovascular disease can benefit from the proper diet and nutrition. Essential vitamins found in the dietary patterns provided by the American Heart Association’s Dietary Guidelines can ultimately help reduce and prevent the risk of cardiovascular disease as well as help improve overall heart health. An improper nutrition consisting of foods rich in saturated and trans fats can increase the prevalence of cardiovascular disease. While diagnosis and drugs/medications can be prescribed to treat cardiovascular disease, a balanced 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 feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
Among the numerous risk factors which can lead to cardiovascular disease and hypertension, dietary and nutritional imbalances are among some of the most prevalent causes behind heart health issues, according to various research studies. While vitamin and mineral deficiencies have been commonly linked to the development of CVD and hypertension, other related compound deficiencies may be just as important towards heart health.
What’s the significance between amino acids and cardiovascular disease?
Many research studies have found a fundamental correlation between the proper intake of amino acids and cardiovascular disease, as well as the increased risk of hypertension. As previously discussed, protein plays a crucial role in almost all biological processes and amino acids are the building blocks of it.�A large proportion of our cells are made up of amino acids, meaning they carry out many important bodily functions, such as giving cells their structure as well as transporting and storing nutrients. Amino acids have an influence on the function of organs, glands, tendons and arteries.
Amino Acids for Cardiovascular Disease
Researchers believe that almost every disease is the result of imbalances to our metabolism and amino acids are mainly responsible for achieving a balanced metabolism.�The objective is that there is a complete amino acid content, maintained in the correct combination. If the one or more amino acids are not available in sufficient quantities, the production of protein is weakened and the metabolism may only function in a limited way. The following are several of the amino acids necessary to sustain overall health and wellness, improving the risk of cardiovascular disease and hypertension.
L-Arginine
L-arginine and endogenous methylarginines are the precursors for the production of NO, or nitric oxide, which has beneficial cardiovascular effects, mediated through conversion of L-arginine to nitric oxide, or NO from eNOS. Patients with hypertension, hyperlipidemia, diabetes mellitus and atherosclerosis have increased levels of HSCRP and inflammation, greater microalbumin, low levels of apelin (stimulates NO in the endothelium), elevated amounts of arginase (breaks down arginine) and increased serum levels of ADMA, which inactivates NO.
Under normal physiological conditions, intracellular arginine levels significantly exceed the Km of eNOS that is less than 5 ?mol. But, endogenous NO formation is dependent on extracellular arginine concentration. The intracellular concentrations of L-arginine are 0.1-3.8 mmol/L in endothelial cells while the plasma concentration of arginine is 80-120 ?mol/L that is about 20-25 times greater than the MMC. Despite this, mobile NO formation depends on exogenous L-arginine and this really is actually the paradox. Arginine can be a more powerful antioxidant and blocks the formation of endothelin, reduces renal sodium reabsorption and modulates BP. The NO production in endothelial cells is closely coupled to arginine uptake indicating that transport mechanics play a significant part in the regulation of function. Arginine can raise vascular and NO bioavailability and influence perfusion, function and BP. Molecular eNOS might occur in the absence of tetrahydrobiopterin which stabilizes eNOS, which leads to production of ROS.
Individual studies in hypertensive and normotensive subjects of L-arginine of parenteral and oral administrations demonstrate an antihypertensive effect as well as progress in coronary artery blood flow and peripheral blood circulation in PAD. The BP decreased by 6.2/6.8 mmHg on 10 g/d of L-arginine when provided as a nutritional supplement or even organic foods to a group of hypertensive subjects. Arginine produces a significant decrease in BP and improved impact in normotensive and hypertensive individuals that is comparable in magnitude to that plan. Arginine awarded in g/d also significantly reduced BP in women with gestational hypertension without proteinuria, decreased the demand for anti-hypertensive therapy, decreased maternal and neonatal complications and protracted the maternity. The combination of arginine (1200 mg/d) and N-acetyl cysteine (NAC) (600 mg bid) administered over 6 mo to hypertensive patients with type 2 diabetes, lowered SBP and DBP (p < 0.05), greater HDL-C, diminished LDL-C and oxLDL, decreased HSCRP, ICAM, VCAM, PAI-I, fibrinogen and IMT. An analysis of 54 hypertensive subjects given grams three times every day for four weeks had significant reductions in 24 h ABM. A meta-analysis of 11 trials with 383 subjects administered arginine 4-24 g/d discovered average reduction in BP of 5.39/2.66 mmHg (p < 0.001) in 4 wk. Although these doses of L-arginine seem to be secure, no long term studies in humans have been released at this time and there are worries of a pro-oxidative influence or even an increase in mortality in individuals who might have severely dysfunctional endothelium, advanced atherosclerosis, CHD, ACS or MI. In addition to the path, there is an pathway that is connected to nitrates out of berries, beetroot juice along with the DASH diet which are converted into nitrites by salivary symbiotic, GI and oral bacteria. Administration of extract or beetroot juice at 500 mg/d improve endothelial function and lower BP, increases nitrites, increase peripheral, coronary and cerebral blood flow.
L-Carnitine and Acetyl-L-Carnitine
L-carnitine is a nitrogenous muscle. Animal studies suggest that carnitine has both hereditary anti-hypertensive effects and anti-oxidant consequences in the heart by up-regulation of both eNOS and PPAR gamma, inhibition of RAAS, modulation of NF-?B and down regulation of NOX2, NOX4, TGF-? and CTGF that reduces vascular fibrosis. While BP and cognitive stress are reduced, endothelial NO function and oxidative defense are improved.
Studies on the effects of L-carnitine and acetyl-L-carnitine are limited. In patients with MS, acetyl-L-carnitine, improved dysglycemia and decreased SBP from 7-9 mmHg, but diastolic BP was significantly decreased only in people with sugar. Low amounts are correlated with a nondipping BP routine in Type 2 DM. Carnitine might be beneficial in the treatment of essential hypertension, type II DM with hyperlipidemia, hypertension, cardiac arrhythmias, CHF and cardiac ischemic syndromes and has anti-inflammatory and antioxidant results. Doses of 2-3 grams per day are recommended.
Taurine
Taurine is a sulfonic acid that is regarded as a conditionally-essential amino acid, which is not used in protein synthesis, but is located free or in easy peptides with its concentration in the brain, retina and myocardium. In cardiomyocytes, it has a role of inotropic factor, an osmoregulator and agent and reflects approximately 50 percent of the amino acids.
Human studies have noted that essential hypertensive subjects have reduced urinary taurine as well as other sulfur amino acids. Taurine lowers BP, SVR and HR, reduces arrhythmias, CHF symptoms and SNS activity, raises urinary sodium and water excretion, raises atrial natriuretic factor, improves insulin resistance, raises NO and improves endothelial function. Taurine also decreases A-II, PRA, aldosterone, SNS activity, plasma norepinephrine, plasma and urinary epinephrine, lowers homocysteine, enhances insulin sensitivity, kinins and acetyl choline responsiveness, reduces intracellular sodium and calcium, reduces reaction to beta receptors and has antioxidant, anti-atherosclerotic and anti-inflammatory activities, reduces IMT and arterial stiffness and may shield from risk of CHD. There is A urinary taurine associated with greater risk of CVD and hypertension. A study of 31 males with hypertension showed a 26 percent increase in taurine levels and also a 287 percent growth in cysteine levels. The BP reduction of 14.8/6.6 mmHg was proportional to increases in serum taurine and discounts in plasma norepinephrine. Fujita et al revealed a reduction in BP of 9/4.1 mmHg (p< 0.05) in 19 hypertension issues given 6 grams of taurine for 2 days. Taurine has numerous beneficial effects on the cardiovascular system and BP. Taurine’s dose is 2 to 3 g/d at but doses around 6 g/d could be required to reduce BP.
In conclusion, amino acids, as well as proteins in this case, are ultimately essential towards improving cardiovascular disease and hypertension. As the essential building block of a majority of the human body’s biological processes, amino acids, as well as the proper consumption of protein, can help maintain a balanced metabolism in order to continue improving cardiovascular disease and hypertension. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
Protein is an essential part of a balanced nutrition. The human�body utilizes protein to build and repair tissues. Protein is also used to make enzymes, hormones, and other fundamental body chemicals. Protein is an important building block of bones, muscles, cartilage, skin, and blood. However, for many individuals, the source of these proteins can often also be full of saturated fats, and too much of it can increase the risk of cardiovascular disease.
Can protein cause cardiovascular disease and hypertension?
Protein can be found in�chicken, pork, fish, beef, tofu, beans, lentils, yogurt, milk, cheese, seeds, nuts, and eggs. The issue with consuming some of these sources of protein that are rich in saturated fats as well is that such can increase the levels of low-density lipoprotein cholesterol (LDL), or in other words, the “bad” cholesterol. Increased levels of LDL cholesterol have been associated with cardiovascular disease and even hypertension. Research studies focusing on the connection between protein intake and CVD as well as hypertension have been conducted to reveal this correlation.
Protein & Cardiovascular Disease
Observational and epidemiologic studies have demonstrated a decrease in blood pressure, or BP, and a consistent association between a high protein consumption and incident BP. The protein source is an important element when it comes to the effect of blood pressure in the body; where animal protein has become less effective than non-animal or plant protein, especially that in almonds. At the Inter-Salt Study of over 10,000 subjects, individuals who have a dietary protein consumption of about 30 percent over the average had reduced BP by 3.0/2.5 mmHg compared to those that were 30 percent below the average. However, wild or lean animal protein with essential and less saturated fats and fatty acids may decrease CHD, lipids and BP risk.
A meta-analysis supported these findings and also indicated that hypertensive individuals and the elderly have the BP reduction with protein intake. Still another meta-analysis of 40 trials with 3277 patients found reductions in BP of 1.76/1.15 mmHg compared to carbohydrate consumption (p < 0.001). Both vegetable and animal protein significantly and equally reduced BP at 2.27/1.26 mmHg and 2.54/0.95 mmHg respectively. Dietary protein consumption is inversely related to risk for stroke. A randomized cross-over study in 352 adults with pre-hypertension and stageIhypertension found a significant decrease in SBP of 2.0 mmHg with soy protein and 2.3 mmHg with milk protein compared to a high glycemic index diet over each of the 8 wk treatment periods. A non-significant decrease has been in DBP. Another RDB parallel study over 4 weeks of 94 subjects with prehypertension and stageIhypertension found significant reductions on office BP of 4.9/2.7 mmHg in those given a combo of 25 percent protein intake vs the control group awarded 15 percent protein within an isocaloric manner. The protein consisted of pea , 20 percent soy, egg that is 30 percent and isolate. The daily recommended intake of nourishment from many sources is 1.0 to 1.5 g/kg body weight, varying with exercise level, age, renal function and other factors.
Fermented milk supplemented with whey protein concentrate reduces BP in. Administration of 20 g/d of hydrolyzed whey protein nutritional supplement rich in bioactive peptides significantly decreased BP more than 6 weeks from 8.0 � 3.2 mmHg in SBP and 5.5 � 2.1 millimeters in diastolic BP. Milk peptides, which equal caseins and whey proteins, are a rich source of ACEI peptides. Val-Pro-Pro and Ile-Pro-Pro awarded at 5 to 60 mg/d have varying reductions in BP using an average reduction in pooled studies of approximately 1.28-4.8/0.59-2.2 mmHg. Yet recent meta-analysis did not reveal significant reductions in BP in people. Powdered fermented milk using Lactobacillus helveticus given at 12 g/d significantly lowered BP from 11.2/6.5 mmHg in 4 weeks. A dose response study revealed reductions in BP. The response is attributed to fermented milk peptides which inhibit ACE.
Pins et al administered 20 g of whey protein that is hydrolyzed and noticed that a BP reduction of 11/7 mmHg compared to controls. Whey protein is successful in enhancing arterial stiffness, insulin resistance, glucose, lipids and BP. These data indicate that the protein must be hydrolyzed so as to exhibit an antihypertensive effect, and also the maximum BP reaction is dose dependent. Bovine peptides and whey peptides that are protein-derived exhibit ACEI activity. These components comprise B-caseins, B-lg B2-microglobulin, fractions and serum albumin. ACEI peptides are released by the hydrolysis of whey protein isolates. Marine collagen peptides (MCPs) from deep sea fish have anti-hypertensive activity. A double-blind placebo controlled trial in 100 hypertensive subjects with diabetes who received MCPs twice a day for 3 months had significant reductions in DBP and mean. Bonito protein (Sarda Orientalis), from the tuna and mackerel family has natural ACEI inhibitory peptides and reduces BP 10.2/7 mmHg in 1.5 g/d.
Sardine muscle protein, which contains Valyl-Tyrosine (VAL-TYR), significantly lowers BP in hypertensive subjects. Kawasaki et al treated 29 hypertensive subjects with 3 milligrams of VAL-TYR sardine muscle focused extract for four wk and reduced BP 9.7/5.3 mmHg (p < 0.05). Levels of aldosterone and A-Iincreased as serum A-II diminished suggesting that VAL-TYR is a ACEI. BP was considerably lowered in a study using a vegetable drink with protein hydrolysates in 13 weeks.
Soy protein reduces BP in patients in most studies. Soy protein consumption was inversely and significantly correlated with both DBP and SBP in 45694 Chinese girls or more of soy protein within 3 years and the association increased with age. The SBP decrease was 1.9 to 4.9 mm reduced and the DBP 0.9 to 2.2 mmHg lower. However, meta-analysis and trials have shown mixed results on BP to reductions of 7 percent to 10 percent for SBP and DBP with no change in BP. The current meta-analysis of 27 trials found a substantial reduction in BP of 2.21/1.44 mmHg. Some studies suggest improvement in ACEI activity, reduction in inflammation and HS-CRP, cognitive function arterial compliance, decrease in tone activity and reduction in both oxidative stress and levels. Fermented soy at roughly 25 g/d is suggested.
Besides ACEI consequences, protein consumption may also alter responses and induce a natriuretic. Low protein intake coupled with low omega 3 fatty acid intake can lead to hypertension in animal models. The perfect protein intake, based on degree of activity, renal function, stress and other factors, is about 1.0 to 1.5 g/kg daily.
In conclusion, protein is an important part of a balanced diet, however, leaner alternatives containing less amounts of saturated fats are ideal to prevent the risk of cardiovascular disease and hypertension, promoting overall health and wellness. Many individuals consume higher amounts of proteins than necessary. A healthcare professional specializing in diet and nutrition can help you come up with the best nutritional plan for your and your specific health concerns. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
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-?.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-?Band 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 feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
Vascular biology, endothelial and vascular smooth muscle as well as cardiac dysfunction play a primary role in hypertension, cardio-vascular disease and target organ damage. Nutrient-gene interactions and epigenetics are predominant factors in promoting positive and negative effects in cardiovascular health and hypertension. In a series of research studies correlated to cardiovascular disease and hypertension, Dr. Mark C. Houston, MD, discussed the role that vascular biology and nutraceuticals play in relation to treatment of hypertension and cardiovascular disease.
What is the cause of cardiovascular disease and hypertension?
Vascular disease can appropriately be described as the balance between vascular injury and vascular repair (Figure 1). The endothelium is strategically found to be closely associated to the bloodstream as well as the vascular smooth muscle and it is also in charge of discharging a variety of substances in order to preserve vascular homeostasis and health (Figures 2 and 3). Numerous irritations which can provoke damage or harm to the endothelium, can lead to endothelial dysfunction, or ED, and can cause hypertension and other cardiovascular diseases.
Hypertension might be a hemodynamic indication of a damaged or injuried endothelium and vascular smooth muscle which could be connected to definite inflammation responses, oxidative stress and immune dysfunction of the arteries leading to ED, vascular and cardiac smooth muscle disorder, loss of arterial elasticity together with reduced arterial compliance and increased systemic vascular resistance. Hypertension is a significant outcome of the interaction between environmental factors and genetics. Macronutrients and micronutrients are crucial in the regulation of blood pressure, or BP, following target organ damage, or TOD. Nutrient-gene interactions, subsequent gene expression, epigenetics, oxidative stress, inflammation and autoimmune vascular dysfunction have positive or negative influences on vascular biology in humans. Endothelial activation with endothelial dysfunction and vascular smooth muscle breakdown, or VSMD, can ultimately trigger and continue to stimulate the development and growth of hypertension.
Macronutrient and micronutrient deficiencies are extremely common in the general population and may be even more common in individuals with hypertension and cardiovascular disease associated with genetics, environmental factors and even prescription drug and medication usage. These deficiencies have an enormous impact on cardiovascular health issues, such as hypertension, myocardial infarction, or MI, stroke and renal disease. The diagnosis and treatment of those deficiencies will reduce BP and improve ED, vascular biology and health, as well as cardiovascular function.
Epidemiology
Epidemiology,�the branch of medicine that deals with the incidence, distribution, and possible control of diseases and other factors relating to health, emphasizes the role of diet and related nutritional intake when it comes to hypertension and cardiovascular disease. The transition from the Paleolithic diet to our modern diet has produced an outbreak of nutritionally-related diseases (Table 1). Hypertension, atherosclerosis, coronary heart disease, or CHD, MI, congestive heart failure, or CHF, cerebro-vascular accidents, or CVA, renal disease, type 2 diabetes mellitus, or T2DM, metabolic syndrome, or MS, and obesity are several examples of those diseases. Table 1 contrasts intake of nutrients included during the Paleolithic Era and modern time, involved in the regulation of blood pressure, or BP. An unnatural and unhealthy nutritional selection process has been established by evolution from a pre-agricultural, hunter-gatherer milieu into an agricultural, refrigeration society. In sum, diet has changed more than our genetics can adapt.
The human genetic makeup is approximately 99.9 percent that of our Paleolithic ancestors, however our nutritional, vitamin and mineral intakes have vastly changed. The macronutrient and micronutrient variations, oxidative stress from radical oxygen species, or ROS, and radical nitrogen species, or RNS, and inflammatory mediators, such as cell adhesion molecules, or CAMs, cytokines, signaling molecules and autoimmune vascular dysfunction of T cells and B cells, have contributed to the greatest prevalence of hypertension and other cardiovascular diseases through complex nutrient-gene interactions, epigenetic and nutrient-caveolae interactions and nutrient responses with pattern recognition receptors from the endothelium (Figure 4). A decrease in endothelin coupled with endothelial activation, increase in angiotensin II and nitric oxide bioavailability can cause coronary artery disease and vascular disease as well as hypertension. Poor nutrition, together with obesity and a sedentary lifestyle have led to an exponential increase in nutritionally-related ailments. In particular, the high Na+/K+ ratio of contemporary diets has contributed to hypertension, CVA, CHD, MI, CHF and renal disorder as have the relatively low intake of omega-3 PUFA, increase in omega-6 PUFA, saturated fat and trans fatty acids.
Pathophysiology
Vascular biology plays a major role in the initiation and perpetuation of hypertension. Oxidative stress (both ROS and RNS), inflammation and autoimmune vascular dysfunction (both T cells and B cells) are the primary pathophysiologic and functional mechanisms that cause cardiovascular disease (Figure 5). All three of them are closely interconnected and provide the absolute combination that leads to cardiovascular disease, or CVD, vascular smooth muscle and cardiac dysfunction, hypertension, vascular disease, atherosclerosis and endothelial dysfunction, or ED.
Hypertension is not a disease but is the proper and continuous, unregulated reaction with an exaggerated outcome of the infinite irritations to the blood vessel following environmental-genetic expression patterns and downstream disturbances in which the vascular system is the innocent bystander. This really becomes a maladaptive vascular response that was initially meant to provide vascular defense to the endothelial insults (Figure 6). Hypertension is a vasculopathy, characterized by ED, structural remodeling, vascular inflammation, improved stiffness, decreased distensibility and loss of elasticity. These insults are biomechanical (BP, heartbeat, blood circulation, oscillatory flow, turbu-lence, enhancement, pulse wave velocity and reflected waves) and biohumoral or biochemical which includes all the non-mechanical causes like metabolic, endocrine, nutritional, toxic, infectious and other etiologies.
In addition to the connections for endocrine and nutritional causes of hypertension, infections and toxins can increase blood pressure as well. Various toxins, such as mercury, polychlorinated biphenyls, lead, cadmium, arsenic and iron, also increase BP and CVD. Numerous microbial organisms have also been implicated in hypertension and CHD. All of these irritations lead to the altered vascular structure and function that manifests clinically as hypertension. Patients with hypertension have abnormal microvasculature in the form of inward eutrophic remodeling of the tiny resistance arteries leading to impaired vasodilatory capacity, increased cardiovascular disease, increased media to lumen ratio, decreased maximal organ perfusion and decreased flow reserve, particularly in the heart with decreased coronary flow reserve. Significant functional structural microvascular impairment occurs even before the individual’s blood pressure begins to increase in normotensive offspring of the patients with hypertension, as evidenced by endothelial dysfunction, diminished vasodilation, forearm vascular resistance, diastolic dysfunction, increased left ventricular mass index, increased septal and posterior wall thickness and left untreated hypertrophy. Therefore, the processes underlying the circulatory issues are associated to a vascular phenotype of hypertension that may be determined by early life programming and imprinting which may be compounded by cerebral aging.
In conclusion, vascular biology, endothelial and vascular smooth muscle as well as cardiac dysfunction play a primary role in hypertension, cardio-vascular disease and target organ damage. Then, the epidemiology, or the incidence, distribution, and possible control of diseases and other factors relating to health, emphasizes the role of diet and related nutritional intake when it comes to hypertension and cardiovascular disease. And finally, oxidative stress, inflammation and autoimmune vascular dysfunction are the primary pathophysiologic and functional mechanisms that cause cardiovascular disease. Hypertension is an indication of cardiovascular issues which should be addressed by a healthcare professional.
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By Dr. Alex Jimenez
Additional Topics: Wellness
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