Amino Acids: 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 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 μmol. 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 μmol/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-κB and down regulation of NOX2, NOX4, TGF-β 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 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.