How Amino Acids Can Benefit Cardiovascular Disease | Wellness Clinic
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.
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Rhetoric from the United States government since the early 1990s proclaims that GM foods are no different from their natural counterparts that have existed for centuries. The Food and Drug Administration (FDA) has labeled them �Generally Recognized as Safe,� or GRAS. This status allows a product to be commercialized without any additional testing. According to US law, to be considered GRAS the substance must be the subject of a substantial amount of peer-reviewed published studies (or equivalent) and there must be overwhelming consensus among the scientific community that the product is safe. GM foods had neither. Nonetheless, in a precedent-setting move in 1992 that some experts contend was illegal, the FDA declared that GM crops are GRAS as long as their producers say they are. Thus, the FDA does not require any safety evaluations or labeling of GMOs. A company can even introduce a GM food to the market without telling the agency.
Taylor�s GMO policy needed to create the impression that unintended effects from GM crops were not an issue. Otherwise their GRAS status would be undermined and they would need the extensive testing and labels that are normally required for food additives. But internal memos made public from a lawsuit showed that the overwhelming consensus among the agency scientists was that GM crops can have unpredictable, hard-to-detect side effects. Various departments and experts spelled these out in detail, listing allergies, toxins, nutritional effects, and new diseases as potential dangers. They urged superiors to require long-term safety studies.5 In spite of the warnings, according to public interest attorney Steven Druker who studied the FDA�s internal files, �References to the unintended negative effects of bioengineering were progressively deleted from drafts of the policy statement (over the protests of agency scientists).�6
There are several reasons why GM plants present unique dangers. The first is that the process of genetic engineering itself creates unpredicted alterations, irrespective of which gene is transferred. The gene insertion process, for example, is accomplished by either shooting genes from a �gene gun� into a plate of cells, or using bacteria to infect the cell with foreign DNA. Both create mutations in and around the insertion site and elsewhere.13 The �transformed� cell is then cloned into a plant through a process called tissue culture, which results in additional hundreds or thousands of mutations throughout the plants� genome. In the end, the GM plant�s DNA can be a staggering 2-4% different from its natural parent.14 Native genes can be mutated, deleted, or permanently turned on or off. In addition, the insertion process causes holistic and not-well-understood changes among large numbers of native genes. One study revealed that up to 5% of the natural genes altered their levels of protein expression as a result of a single insertion.
The very first crop submitted to the FDA�s voluntary consultation process, the FlavrSavr tomato, showed evidence of toxins. Out of 20 female rats fed the GM tomato, 7 developed stomach lesions.21 The director of FDA�s Office of Special Research Skills wrote that the tomatoes did not demonstrate a �reasonable certainty of no harm,�22 which is their normal standard of safety. The Additives Evaluation Branch agreed that �unresolved questions still remain.�23 The political appointees, however, did not require that the tomato be withdrawn.1
GM Diets Cause Liver Damage
GM Fed Animals Had Higher Death Rates & Organ Damage
About two dozen farmers reported that their pigs had reproductive problems when fed certain varieties of Bt corn. Pigs were sterile, had false pregnancies, or gave birth to bags of water. Cows and bulls also became sterile. Bt corn was also implicated by farmers in the deaths of cows, horses, water buffaloes, and chickens.55
Allergic reactions occur when the immune system interprets something as foreign, different, and offensive, and reacts accordingly. All GM foods, by definition, have something foreign and different. And several studies show that they provoke reactions. Rats fed Monsanto�s GM corn, for example, had a significant increase in blood cells related to the immune system.58 GM potatoes caused the immune system of rats to respond more slowly.59 And GM peas provoked an inflammatory response in mice, suggesting that it might cause deadly allergic reactions in people.60
For years, organic farmers and others have sprayed crops with solutions containing natural Bt bacteria as a method of insect control. The toxin creates holes in their stomach and kills them. Genetic engineers take the gene that produces the toxin in bacteria and insert it into the DNA of crops so that the plant does the work, not the farmer. The fact that we consume that toxic pesticide in every bite of Bt corn is hardly appetizing.
Although the number of safety studies on GM foods is quite small, it has validated the concerns expressed by FDA scientists and others. Unfortunately, government safety assessments worldwide are not competent to even identify most of the potential health problems described above, let alone protect its citizens from the effects.88
Submissions to the US Food and Drug Administraion (FDA) may be worse than in other countries, since the agency doesn�t actually require any data. Their policy says that biotech companies can determine if their own foods are safe. Anything submitted is voluntary and, according to former Environmental Protection Agency scientist Doug Gurian-Sherman, PhD, �often lack[s] sufficient detail, such as necessary statistical analyses needed for an adequate safety evaluation.� Using Freedom of Information Requests, Dr. Gurian-Sherman analyzed more than a fourth of the data summaries (14 of 53) of GM crops reviewed by the FDA. He says, �The FDA consultation process does not allow the agency to require submission of data, misses obvious errors in company- submitted data summaries, provides insufficient testing guidance, and does not require sufficiently detailed data to enable the FDA to assure that GE crops are safe to eat.�94 Similarly, a Friends of the Earth review of company and FDA documents concluded:
The unpublished industry studies submitted to regulators are typically kept secret based on the claim that it is �confidential business information.� The Royal Society of Canada is one of many organizations that condemn this practice. They wrote:
In addition, to relying on untested assumptions, industry-funded research is often designed specifically to force a conclusion of safety. In the high lysine corn described above, for example, the levels of certain nutritional components (i.e. protein content, total dietary fiber, acid detergent fiber, and neutral detergent fiber) were far outside the normal range for corn. Instead of comparing their corn to normal controls, which would reveal this disparity, Monsanto compared it to obscure corn varieties that were also substantially outside the normal range on precisely these values. Thus, their study found no statistical differences by design.
Monsanto�s 1996 Journal of Nutrition studies on Roundup Ready soybeans107,108 provide plenty of examples of scientific transgressions. Although the study has been used often by the industry as validation for safety claims, experts working in the field were not impressed. For example, Dr. Arpad Pusztai was commissioned at the time by the UK government to lead a 20 member consortium in three institutions to develop rigorous testing protocols on GM foods�protocols that were never implemented. Dr. Pusztai, who had published several studies in that same nutrition journal, said the Monsanto paper was not �up to the normal journal standards.� He said, �It was obvious that the study had been designed to avoid finding any problems. Everybody in our consortium knew this.� Some of the flaws include:
When governments fail in their duty to keep corporations in check, the �protector� role should shift to the media, which acts as a watchdog to expose public dangers and governmental shortcomings. But mainstream media around the world has largely overlooked the serious problems associated with GM crops and their regulation. The reason for this oversight is varied and includes contributions from an aggressive public relations and disinformation campaign by the biotech industry, legal threats by biotech companies, and in some cases, the fear of losing advertising accounts. This last reason is particularly prevalent among the farm press, which receives much of its income from the biotech industry.
One of the most troubling aspects of the biotech debate is the attack strategy used on GMO critics and independent scientists. Not only are adverse findings by independent scientists often suppressed, ignored, or denied, researchers that discover problems from GM foods have been fired, stripped of responsibilities, deprived of tenure, and even threatened. Consider Dr. Pusztai, the world�s leading scientist in his field, who inadvertently discovered in 1998 that unpredictable changes in GM crops caused massive damage in rats. He went public with his concerns, was a hero at his prestigious institute for two days, and then, after the director received two phone calls allegedly from the UK Prime Minister�s office, was fired after 35 years and silenced with threats of a lawsuit. False statements were circulated to trash his reputation, which are recited by GMO advocates today.
Since GM foods are not properly tested before they enter the market, consumers are the guinea pigs. But this doesn�t even qualify as an experiment. There are no controls and no monitoring. Given the mounting of evidence of harm, it is likely that GM foods are contributing to the deterioration of health in the United States, Canada, and other countries where it is consumed. But without post- marketing surveillance, the chances of tracing health problems to GM food are low. The incidence of a disease would have to increase dramatically before it was noticed, meaning that millions may have to get sick before a change is investigated. Tracking the impact of GM foods is even more difficult in North America, where the foods are not labeled.
It was during the period between 1910 and 1920 when it was suggested for the first time that a cluster of associated metabolic disturbances tended to coexist together [1]. Since then, different health organisms have suggested diverse definitions for metabolic syndrome (MetS) but there has not yet been a well-established consensus. The most common definitions are summarized in Table 1. What is clear for all of these is that the MetS is a clinical entity of substantial heterogeneity, commonly represented by the combination of obesity (especially abdominal obesity), hyperglycemia, dyslipidemia and/or hypertension [2�6].
Several dietary strategies and their potential positive effects on the prevention and treatment of the different metabolic complications associated to the MetS, are described below and summarized in Table 2.
2.1. Energy-Restricted Diet Strategies
The very long-chain eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are essential omega-3 polyunsaturated fatty acids (n-3 PUFAs) for human physiology. Their main dietary sources are fish and algal oils and fatty fish, but they can also be synthesized by humans from ?-linolenic acid [40].
Over the last ten years, the concern about the quality of the carbohydrates (CHO) consumed has risen [46]. In this context, the glycemic index (GI) is used as a CHO quality measure. It consists in a ranking on a scale from 0 to 100 that classifies carbohydrate-containing foods according to the postprandial glucose response [47]. The higher the index, the more promptly the postprandial serum glucose rises and the more rapid the insulin response. A quick insulin response leads to rapid hypoglycemia, which is suggested to be associated with an increment of the feeling of hunger and to a subsequent higher caloric intake [47]. The glycemic load (GL) is equal to the GI multiplied by the number of grams of CHO in a serving [48].
Dietary total antioxidant capacity (TAC) is an indicator of diet quality defined as the sum of antioxidant activities of the pool of antioxidants present in a food [55]. These antioxidants have the capacity to act as scavengers of free radicals and other reactive species produced in the organisms [56]. Taking into account that oxidative stress is one of the remarkable unfortunate physiological states of MetS, dietary antioxidants are of main interest in the prevention and treatment of this multifactorial disorder [57]. Accordingly, it is well-accepted that diets with a high content of spices, herbs, fruits, vegetables, nuts and chocolate, are associated with a decreased risk of oxidative stress-related diseases development [58�60]. Moreover, several studies have analyzed the effects of dietary TAC in individuals suffering from MetS or related diseases [61,62]. In the Tehran Lipid and Glucose Study it was demonstrated that a high TAC has beneficial effects on metabolic disorders and especially prevents weight and abdominal fat gain [61]. In the same line, research conducted in our institutions also evidenced that beneficial effects on body weight, oxidative stress biomarkers and other MetS features were positively related with higher TAC consumption in patients suffering from MetS [63�65].
The macronutrient distribution set in a weight loss dietary plan has commonly been 50%�55% total caloric value from CHO, 15% from proteins and 30% from lipids [57,68]. However, as most people have difficulty in maintaining weight loss achievements over time [69,70], research on increment of protein intake (>20%) at the expense of CHO was carried out [71�77].
The concept of the 
New studies focused on the molecular action of nutritional bioactive compounds with positive effects on MetS are currently an objective of scientific research worldwide with the aim of designing more personalized strategies in the framework of molecular nutrition. Among them, flavonoids and antioxidant vitamins are some of the most studied compounds with different potential benefits such as antioxidant, vasodilatory, anti-atherogenic, antithrombotic, and anti-inflammatory effects [119]. Table 3 summarizes different nutritional bioactive compounds with potential positive effects on MetS, including the possible molecular mechanism of action involved.
Vitamin C, ascorbic acid or ascorbate is an essential nutrient as human beings cannot synthesize it. It is a water-soluble antioxidant mainly found in fruits, especially citrus (lemon, orange), and vegetables (pepper, kale) [120]. Several beneficial effects have been associated to this vitamin such as antioxidant and anti-inflammatory properties and prevention or treatment of CVD and type 2 diabetes [121�123].
Hydroxytyrosol (3,4-dihydroxyphenylethanol) is a phenolic compound mainly found in olives [132].
Quercetin is a predominant flavanol naturally present in vegetables, fruits, green tea or red wine. It is commonly found as glycoside forms, where rutin is the most common and important structure found in nature [141].
Tocopherols, also known as vitamin E, are a family of eight fat-soluble phenolic compounds whose main dietary sources are vegetable oils, nuts and seeds [130,158].
Catechins are polyphenols that can be found in a variety of foods including fruits, vegetables, chocolate, wine, and tea [175]. The epigallocatechin 3-gallate present in tea leaves is the catechin class most studied [176].
PubMed was searched from the earliest possible date to May 2014 to identify review articles that outlined the pathophysiology of MetS and T2DM. This led to further search refinements to identify inflammatory mechanisms that occur in the pancreas, adipose tissue, skeletal muscle, and hypothalamus. Searches were also refined to identify relationships among diet, supplements, and glycemic regulation. Both animal and human studies were reviewed. The selection of specific supplements was based on those that were most commonly used in the clinical setting, namely, gymnema sylvestre, vanadium, chromium and ?-lipoic acid.
Under normal conditions, skeletal muscle, hepatic, and adipose tissues require the action of insulin for cellular glucose entry. Insulin resistance represents an inability of insulin to signal glucose passage into insulin-dependent cells. Although a genetic predisposition can exist, the�etiology of insulin resistance has been linked to chronic low-grade inflammation.1 Combined with insulin resistance-induced hyperglycemia, chronic low-grade inflammation also sustains MetS pathophysiology.1
Caloric excess and a sedentary lifestyle contribute to the accumulation of subcutaneous and visceral adipose tissue. Adipose tissue was once thought of as a metabolically inert passive energy depot. A large body of evidence now demonstrates that excess visceral adipose tissue acts as a driver of chronic low-grade inflammation and insulin resistance.27,34
Eating behavior in the obese and overweight has been popularly attributed to a lack of will power or genetics. However, recent research has demonstrated a link between hypothalamic inflammation and increased body weight.41,41
Feeding generally leads to a short-term increase in both oxidative stress and inflammation. 41 Total�calories consumed, glycemic index, and fatty acid profile of a meal all influence the degree of postprandial inflammation. It is estimated that the average American consumes approximately 20% of calories from refined sugar, 20% from refined grains and flour, 15% to 20% from excessively fatty meat products, and 20% from refined seed/legume oils.45 This pattern of eating contains a macronutrient composition and glycemic index that promote hyperglycemia, hyperlipemia, and an acute postprandial inflammatory response. 46 Collectively referred to as postprandial dysmetabolism, this pro-inflammatory response can sustain levels of chronic low-grade inflammation that leads to excess body fat, coronary heart disease (CHD), insulin resistance, and T2DM.28,29,47
Diagnosis of MetS has been linked to an increased risk of developing T2DM and cardiovascular disease over the following 5 to 10 years. 1 It further increases a patient’s risk of stroke, myocardial infarction, and death from any of the aforementioned conditions.1
Research has identified nutrients that play key roles in promoting proper insulin sensitivity, including vitamin D, magnesium, omega-3 (n-3) fatty acids, curcumin, gymnema, vanadium, chromium, and ?-lipoic acid. It is possible to get adequate vitamin D from sun exposure and adequate amounts of magnesium and omega-3 fatty acids from food. Contrastingly, the therapeutic levels of chromium and ?-lipoic acid that affect insulin sensitivity and reduce�insulin resistance cannot be obtained in food and must be supplemented.
Vitamin D, magnesium, and n-3 fatty acids have multiple functions, and generalized inflammation reduction is a common mechanism of action.74�80 Their supplemental use should be considered in the context of low-grade inflammation reduction and health promotion, rather than as a specific treatment for MetS or T2DM.
Gymnemic acids are the active component of the G sylvestre plant leaves. Gymnemic acids are the active component of the G sylvestre plant leaves. Studies evaluating G sylvestre’s effects on diabetes in humans have generally been of poor methodological quality. Experimental animal studies have found that gymnemic acids may decrease glucose uptake in the small intestine, inhibit gluconeogenesis, and reduce hepatic and skeletal muscle insulin resistance.99 Other animal studies suggest that gymnemic acids may have comparable efficacy in reducing blood sugar levels to the first-generation sulfonylurea, tolbutamide.100
Vanadyl sulfate has been reported to prolong the events of insulin signaling and may actually improve insulin sensitivity.101 Limited data suggest that it inhibits gluconeogenesis, possibly ameliorating hepatic insulin resistance. 100,101 Uncontrolled clinical trials have reported improvements in insulin sensitivity using 50 to 300 mg daily for periods ranging from 3 to 6 weeks. 101�103 Contrastingly, a recent randomized, double-blind, placebo-controlled trial found that 50 mg of vanadyl sulfate twice daily for 4 weeks had no effect in individuals with impaired glucose tolerance. 104 Limited clinical and experimental data exist supporting the use of vanadyl sulfate to improve insulin resistance,�and further research is warranted regarding its safety and efficacy.
Diets high in refined sugar and flour are deficient in chromium (Cr) and lead to an increased urinary excretion of chromium. 105,106 The progression of MetS is not likely caused by a chromium deficiency, 107 and dosages that benefit glycemic regulation are not achievable through food. 106,108,109
Humans derive ?-lipoic acid through dietary means and from endogenous synthesis. 111 The foods richest in ?-lipoic acid are animal tissues with extensive metabolic activity such as animal heart, liver, and kidney, which are not consumed in large amounts in the typical American diet. 111 Supplemental amounts of ?-lipoic acid used in the treatment of T2DM (300-600 mg) are likely to be as much as 1000 times greater than the amounts that could be obtained from the diet.112
This is a narrative overview of the topic of MetS. A systematic review was not performed; therefore, there may be relevant information missing from this review. The contents of this overview focuses on the opinions of the authors, and therefore, others may disagree with our opinions or approaches to management. This overview is limited by the studies that have been published. To date, no studies have been published that identify the effectiveness of a combination of a dietary intervention, such as the Spanish 
