Preventing cardiovascular disease: the SAD problem
Despite recent unearthing of the saturated fat hoax, bankrolled for decades by industrial food makers, there is still a lot of generic narrative out there addressing the prevention of cardiovascular disease as if it boiled down to a mere war on cholesterol - a snap, thanks to mass-produced breakfast cereals and medications, isn’t it? This is obviously a die-hard vestige of six or more decades of deceitful persuasion, which tricked us all into holding saturated fats and dietary cholesterol single-handedly accountable for heart attacks and vascular thromboses. It is easily conceivable that much commercial journalism may not yet be ready to forfeit that kind of quick and profitable attention. However, while reaching all segments of the population cannot happen overnight, new findings are beginning to rattle the foundations of ambiguous processed food manufacturers in America, and exposing their crafty propaganda. Incontrovertible data from large cohort studies point to lifestyle factors playing a role in cardiovascular disorders that include vital nutrient deficiencies, sugar addiction, consumption of unhealthy fats, and constant exposure to endocrine disruptors and other chemicals in low-grade animal products and fast foods. The complex and constant interplay of nutrient imbalances and noxious chemicals is what imperils human health: cholesterol plays a part in the story, but is by no means an independent risk factor.
Four major cardiovascular disease risk factors associated with the SAD, or Standard American Diet
[Note: while hypertension and inflammation are not enumerated among the risk factors, as I have outlined them in previous articles, they are designated as collateral implications of all four SAD related risk factors investigated below]
1. Insulin Resistance
It is estimated that 80% of Americans have this metabolic condition, which is still somewhat underdiagnosed. Insulin resistance is an impaired ability to metabolize sugars for energy, caused by long term, continuous refined carbohydrate intake in excess of energy requirements and diets high in processed foods. Persistent insulin flooding in response to frequent sugar intake blunts cell receptors; these begin to ‘shut the door’ on insulin when it tries to usher in glucose molecules to be used for energy. The ousted glucose molecules linger in the bloodstream and cause damage to tissues and organs by attaching to and seizing proteins like hemoglobin, the protein that shuttles oxygen, as well as cholesterol lipoproteins. The real reason for LDL being ominously labeled as the ‘bad’ cholesterol is that it undergoes a Jekyll to Hyde mutation by the hands of sugar. Besieged and sugar-coated LDL cholesterol particles become structurally transfigured and are readily oxidized by free radicals. Since they are rendered unable to carry out their beneficial functions, they land instead in the arteries to form dangerous plaque. We have seen how LDL-reducing statin medications, though partially (and arguably) supportive for the long term, cannot prevent or halt the genesis of glycated/oxidized LDL, much less reduce its load. Statistically, two thirds of all heart attacks happen to individuals who have insulin related metabolic dysfunctions such as pre-diabetes, diabetes and obesity, countless of them being on cholesterol medications, proving that statins are powerless against the damages of sugar.
Hyperinsulinemia (excess plasma insulin relative to the level of glucose), a result of insulin resistance, leads to a condition called Nonalcoholic Fatty Liver Disease (NAFLD), a build-up of fat cells in liver tissue to levels above 5-10% of its weight. NAFLD currently impacts 30% to 40% of Americans and it is an independent risk factor for cardiovascular disease (CVD) and mortality: CVD is one of the most common causes of death among individuals with NAFLD. Because of that, management of this insulin resistance related condition must include a comprehensive preventive strategy for cardiovascular disease. Risk factors such as dyslipidemia (high/oxidized LDL, high triglycerides, too high or too low HDL), diabetes mellitus, hypertension, smoking and poor nutrition must be properly managed to prevent cardiac events and death in individuals with NAFLD.
Insulin resistance is also a cause of systemic inflammation, due to the ensuing accrual of excess visceral fat, which secretes inflammatory chemicals called adipose cytokines. Inflammation and fatty liver, in turn, make insulin receptors less sensitive, in a vicious cycle, and increase oxidative stress, which is a major contributing cause to atherosclerosis. Inflammation also causes existing vulnerable plaque in the arteries to become more prone to rupturing, even in cases when the arteries present minor blockage (a small amount of plaque), and it makes the blood more prone to clotting, leading to heart attacks and strokes.
On one last important note, insulin resistance is a direct cause of sodium retention and consequent hypertension. The cells in our body are equipped with a mechanism called ‘sodium-potassium pump’ that manages cellular exchanges of sodium and potassium. Under normal insulin state, functioning kidneys will filter a teaspoon of salt (2300 mg) every five minutes, adding up to a traffic of 3 to 4 pounds of salt, in the kidneys, per day. If cells are shutting the door on insulin, potassium, which uses insulin as a carrier (much like glucose) cannot enter the cell environment, causing an imbalance that results in an excess of sodium trapped inside the cells; the kidneys, when that happens, hold on to as much salt as they can in a conservation effort, because they do not detect sodium in the blood coming through, and blood pressure is raised in an effort to upregulate plasma volume.
Testing for Insulin Resistance
Insulin resistance can occur long before it impacts blood glucose, which makes specific testing indispensable. While your waist to height ratio (waist divided by height) being over .53 can be a good indicator of insulin resistance because of visceral fat, there is no accurate substitute for a blood test. Following are some of the most reliable assessment methods:
Insulin Response Test, the most important indicator of the presence and severity of diabesity, rarely done in medical practices today unless it is requested. It tests both glucose and insulin.
Homa IR test (Homeostatic Model Assessment of Insulin Resistance), which takes into account the ratio of insulin to glucose, by assessing how much insulin is produced by the pancreas in response to glucose. The higher your score is, the harder your pancreas is working to spew out insulin in an effort to compensate.
CardioIQ® Insulin Resistance Panel with Score which measures levels of insulin and C-peptide, co-secreted from pancreatic β-cells.
HgA1c, or glycosylated hemoglobin provides a 3 month-average glucose level by detecting glucose attached to red blood cells (the life span of a red blood cell is about 3 months). Home testing kits are available online. However, this test may fail to be 100% accurate since you may have insulin resistance and still have normal blood sugar levels.
The triglyceride-to-HDL ratio on a lipid panel is an easy, great predictor of insulin resistance. Triglycerides are blood lipids that are made by the liver to store unused calories, particularly those coming from a high carbohydrate diet, that are meant to be released for energy in a fasting state. Hypertriglyceridemia, and a ratio to HDL between 2 and 3, regardless of LDL values, may signal an incipient problem; a ratio over 3 is a marker for advanced insulin resistance, and a pro-inflammatory pattern. Below are reference ranges for triglycerides in adults:
Normal: Less than 150 mg/dL
Borderline: 150 to 199 mg/dL
High: 200 to 499 mg/dL
Very High: 500 mg/dL or above
2. Low or dysfunctional HDL
HDL stands for High Density Lipoprotein, affectionately named ‘good cholesterol’ and touted as the safeguard of cardiac health. Like LDL, HDL is also primarily made by the liver, and its most valiant mission is indeed to raid unneeded LDL out of the cells, on a return pathway called Reverse Cholesterol Transport, also termed Cholesterol Efflux Capacity. Under optimal conditions, the lipoprotein portion of HDL, once it has released its own lipid load, seizes residual LDL from the cells around the body and transports it back to the liver, which expels it into the bile for complete excretion through the feces. Recent epidemiological studies have subverted the theory that the higher the level of HDL, the lower the odds of obstructive coronary heart disease, and scientists now dissent from the idea that larger particles are more efficient at preventing adverse outcomes, concluding that the true value of HDL in terms of its protective effects correlates with particle number and size, and their degree of functionality. Problems in fact arise when HDL’s functionality is blunted due to poor dietary choices, such as in the standard American diet, which causes LDL to accumulate in the cells and its particles to change unfavorably into the small, dense kind – the atherogenic, or plaque-causing one.
HDL is a complex compound made up of over 100 different molecules such as lipids, amino-acids, protein and antioxidants. The chemical versatility of HDL, when its functionality is optimal, is what makes it so valuable: it has both antiatherogenic and antithrombotic properties, in that it not only helps prevent plaque from forming by cleaning up excess LDL, but through its antioxidant and anti-inflammatory actions it also makes vulnerable plaque (the ‘softer’ kind) more stable, meaning less prone to sudden rupturing, which is a cause of myocardial infarctions even in seemingly healthy and younger individuals. HDL may provide potent protection of LDL in vivo from oxidative damage, induced by free radicals inside the arteries; it also exerts vascular protective effects by upregulating endothelial nitric oxide, a molecule that modulates vascular contractility and averts narrowing of the arteries and blood clots, facilitating blood flow. HDL is also able to counteract calcification of the harder kind of occlusive plaque, the one that forms over long periods of time and causes heart attacks in older individuals.
Functional testing: why more HDL is not always better
Conventional lab tests assess blood levels of LDL, HDL and Triglycerides, not the size and activity of cholesterol particles. HDL Function test is one of the most innovative tests available to measure HDL Functionality. As alluded to before, studies and clinical research have defied the long-standing notion that higher HDL levels are invariably protective, and found instead an association between high levels of HDL and occlusive cardiovascular disease risk.
High HDL, in excess of 50/55 in men, and 65/70 in women, signals that the particles may not be functioning at their best and are possibly being overproduced in a compensatory effort. HDL may in fact lose its protective abilities under certain conditions, such as when high levels of myeloperoxidase (MPO) are present. MPO is an enzyme released by white blood cells called macrophages in response to inflammation and infections. Testing MPO levels gauges the body’s response to damaged artery walls that have become flimsy and cracked due to oxidized and inflamed cholesterol particles lodged in the artery walls. When released, MPO has a dual damaging action: it initiates an attack to LDL particles inside the artery walls since it perceives them as pathogens, causing white blood cells to attach to them and form foam cells that accumulate as plaque, but also modifies and oxidizes the HDL lipoprotein coating, making it dysfunctional. High levels of MPO are a surefire marker for dysfunctional HDL.
Low HDL , at values <30, a component of metabolic syndrome, is invariably predictive of cardiovascular risk. However, clinical trials have shown therapeutically increased HDL levels do not reduce rates of cardiovascular events, simply because increasing its availability through medications does not translate into higher functionality. In conclusion, although genetic factors and health conditions may play a role, the efficiency of all the molecules composing HDL, which is what gives it the ability to carry out a wide spectrum of protective biological functions, is critically dependent on the quality of our diet and lifestyle. Dietary modifications, as well as nutraceuticals clinically proven to aid in upregulating HDL functionality, are outlined in the “Preventing cardiovascular disease: a nutrition design”.
3. Homocysteine
Homocysteine is an amino-acid, made in our body from the breakdown of ingested proteins, that doctors are testing with increasing frequency because, at high levels, it is considered an independent marker for cardiovascular disease, heart attacks and strokes. Anytime we ingest protein foods our metabolism breaks those proteins down into its ‘Lego’ pieces, called amino acids, to later reassemble them into proteins as needed, in order to carry out myriads of diverse functions around the body. One of the amino-acids contained primarily in meat protein, called methionine, gets converted to homocysteine in our body through a biochemical cycle called methylation, that relies on an enzyme called MTHFR (methylenetetrahydrofolate reductase). For methylation to occur, methionine first turns into an active form called Sam-e, (s-adenosylmethionine); Sam-e is hence the first step of conversion of methionine to homocysteine and acts as a methyl donor, meaning it provides the enzymes necessary for the full methylation, or conversion.
Homocysteine has some important functions such as assisting in making cellular energy and making glutathione, the master antioxidant of the human body. The last step of the methionine cycle is the conversion of homocysteine back to methionine, which is crucial because if levels of homocysteine run too high, it goes from good to bad, turning into a noxious compound. Adequate levels of all the B vitamins, particularly B2, B6, B12 and Folate (B9) must be optimal in order to complete the cycle back to methionine. From a nutrition standpoint, poor intake of foods naturally containing these B vitamins, a diet too high in protein - hence more methionine than the body can handle - and excessive coffee intake, can all contribute to increased homocysteine levels, though other factors may adversely affect the methylation process, such as certain medications like proton pump inhibitors, commonly prescribed for acid reflux.
Some of the effects of high homocysteine levels leading to cardiovascular disease:
vascular damage
increased blood clotting
oxidative stress
unruly inflammation
damage to DNA
neurotoxicity
alterations in neurotransmitter pathways
reduced detoxification
reduced endogenous antioxidant production
microalbuminuria, an abnormal protein in the urine that indicates a high risk for cardiovascular disease as well as kidney dysfunction
atherosclerosis, due to reduced elasticity of the arteries and increased production of stiffer collagen fibers in the vascular system
hypertension, because it downregulates blood vessel dilation
Testing for homocysteine:
A simple blood test performed clinically is enough to determine levels of homocysteine. This test must be performed in a fasting state for accurate results; ingestion of any protein prior to the test can skew results. Normal range is between 5 and 15 umol/L, however a growing body of evidence seems to point to levels above 8 as a risk factor in cardiovascular disease. In fact, all of the risks for negative health outcomes seem to be lowest at the 6-8 umol/L mark. However, low levels of homocysteine (hypohomocysteinemia) can also have negative health consequences, primarily because homocysteine is needed to manufacture our ‘master antioxidant’, glutathione, one of our prime defenses against oxidative stress, inflammation and nerve damage. Low levels are associated with many chronic pathologies.
Abnormalities in homocysteine levels may also be caused by a mutation in the MTHFR gene, which instructs the body to make an enzyme that converts dietary folic acid into its biologically active form, methyl-folate. Methyl-folate is critical to methylation, a biochemical mechanism that helps to optimize a huge number of processes in the body, including the production of DNA, metabolism of hormones, and proper detoxification. Between 30 and 60 percent of all people may carry an MTHFR gene variant which leads to low levels of folate and B vitamins, impedes proper metabolism and absorption of vitamins, minerals and proteins, and causes levels of homocysteine to rise in the blood. A DNA test can detect the variant, however, testing for MTHFR mutation is only recommended to women who are trying to conceive and people with treatment-resistant depression, since folate plays a role in regulating neurotransmitter production. The rest of us can simply modify our diets to include nutrients that support MTHFR, simply because, whether or not you have a normal MTHFR gene expression, other overwhelmingly common factors may still be causing high homocysteine, such as:
processed foods
unhealthy fats
lack of zinc and antioxidants
sedentary lifestyle
smoking
excessive alcohol intake
diabetes
chronic inflammatory diseases
celiac disease
Crohn’s disease
thyroid imbalances
long-term use of PPIs, steroid medications, and Metformin (it blocks B12 absorption)
cholesterol lowering medications
long term use of anti-epileptic drugs
excessive intake of protein
large amounts of coffee (more than one cup per day)
4. Low magnesium and potassium, high calcium, misunderstood sodium
Our cardiovascular health (and for that matter, our health in general) is much more dependent on our intake of minerals than we would imagine, but since the bulk of medical research is sponsored by pharmaceutical companies, we are simply not told how crucial these micronutrients are in human pathology. Electrolyte imbalances are possibly the most underestimated plight in the SAD, though awareness is certainly growing, thanks to the work of some notable researchers.
In a recently published book called ‘The Salt Fix’, Dr. James Dinicolantonio, a Doctor of Pharmacy and renowned cardiovascular research scientist whose research focuses primarily on imbalances in the SAD, has brilliantly dispelled the long standing belief that high sodium intake is a major determinant, in and for itself, for the risk of cardiovascular events. Sodium, he says, is an efficient vasodilator, it decreases heart rate and increases circulation; the majority of the US population lacks two important minerals because of the SAD diet, specifically because of insulin resistance: potassium and magnesium. His leading hypothesis, corroborated by epidemiological studies and experimental trials, is that a diet high in sugar and carbohydrates is the actual cause of electrolyte disarray, because insulin resistance prevents these two minerals from getting into the cells and balancing out, respectively, sodium and calcium.
Dr. Carolyn Dean, a Medical Doctor and Naturopath who has been researching magnesium for 40 years, maintains that the lack of magnesium in our modern diet is the cause of a myriad of conditions that allopathic medicine is ironically treating with medications that impoverish magnesium reserves in the body. Her book ‘The Magnesium Miracle’ highlights the importance of this mineral that is involved in nearly 800 functions in the body, many of which relate to cardiovascular health. Magnesium and potassium deficiencies exert comparable damaging effects on the heart. Fact is, it is nearly impossible to increase potassium without replacing magnesium. One of the reasons why electrolyte treatments in hospitals fail to work, is because in most clinical settings they look at sodium, potassium, calcium and chloride and do not include magnesium in the mix.
Calcium, the most abundant mineral in the body, has a big job in the electrical system of the heart. Calcium molecules enter the 3 billion heart muscle cells during heartbeats and help to coordinate the pumping activity by regulating muscle contractility: every time the heart muscle contracts, it then pumps out blood to the rest of the body. The electric signal sparked by calcium particles travels through heart cells like a ripple wave: an electric signal travels from cell to cell, with each cell jolting the next. Once the calcium molecules are removed from heart cells, the heart muscle relaxes, allowing the heart ventricles to refuel on blood and then pump it out again. But calcium has an even greater responsibility, in that it regulates the activity of receptors on the heart cells that let other minerals in, like sodium, potassium and chloride. Abnormalities in calcium levels, due to malfunction of heart cell receptors, can cause a cluster of dysfunctions called heart rhythm disorders like atrial fibrillation, or AFib, a condition in which the electrical activity of the heart becomes erratic and uncoordinated, leading to scarce blood supply to the organs. AFib is treated in conventional medicine with a class of drugs called calcium channel blockers. Interestingly enough, the ion channels that allow calcium to enter and leave the cells are regulated by magnesium. It is magnesium that flushes extra calcium out of muscle or nerve cells to prevent excessive contraction, acting as a natural channel blocker. Paradoxically, calcium channel blocker drugs lower magnesium!
There is a plethora of evidence that Sudden Cardiac Arrest is also related to magnesium deficiency. SCA differs from heart attacks in that the heart suddenly stops beating, impeding blood going to the brain and other organs: if not treated within minutes, the person will die. the majority of sudden cardiac arrests comes from arrhythmias, which, as discussed above, denote less than functional levels of magnesium to antagonize calcium. Drugs like Lasix, a powerful diuretic, and PPIs, Proton Pump Inhibitors (prescribed for gastric disorders) deplete the body of minerals like magnesium and potassium, and consistent use may hence be deemed a predictor for heart problems.
Indeed, calcium excess and magnesium deficiency in the Western diet may be the neglected, underlying precondition to a score of chronic ills. The ratio of calcium to magnesium must be positively maintained at 1:1. The fallacious belief that it should be at 2:1 is the product of mistranslated recommendations by a French scientist in 1989. Current dietary ratio of calcium to magnesium in America is an appalling 10:1, due to the overarching calcium propaganda and consequent ‘fetching’ fortification of processed foods and arbitrary supplementation, as well as the widespread use of anti-acids and common drugs that lower magnesium, driving calcium levels through the roof. The propaganda for Vitamin D has also played a role in this, since Vitamin D boosts absorption of calcium, and in the absence of adequate magnesium, it may freely overegg the pudding.
The issue with hypertension, a major risk factor associated with cardiac health, relates to insufficient potassium from both soil depletion and inadequate intake in the American diet, as well as to insulin resistance: these two diet-related imbalances are strictly interdependent, in that potassium relies on insulin to be ferried into cells. You can read more about the main causes of hypertension here and here.
In conclusion, as the SAD scale negatively tips in favor of sodium and calcium, it is the deficiency of their respective antagonists, potassium and magnesium, that constitutes the real problem.
Testing for potassium and sodium
An electrolyte panel, routinely run in clinical settings as part of a comprehensive metabolic panel, can assess the levels of potassium along with sodium, chloride and bicarbonate. A normal potassium range is between 3.6 and 5.2 millimoles per liter (mmol/L) of blood. A normal blood sodium level is between 135 and 145 milliequivalents per liter (mEq/L).
A urine potassium test can also be performed to gauge levels. Normal urine potassium values are generally 20 mEq/L in a random urine sample and 25 to 125 mEq per day in a 24 hour collection.
Testing for magnesium
I will begin by pointing out that supplementing with magnesium is extremely safe, and most people do not need to test their levels. The body naturally excretes magnesium for two reasons: 1. it is in excess or 2. the supplement used is not of high quality and therefore not highly absorbable (hence its laxative effect). Supplementing, provided a good product is chosen, is always a good idea, particularly in this day and age with our diets being easily conducive to deficiencies or losses.
Routine electrolyte panels do not include magnesium. For those who still wish to gauge their levels, magnesium testing can be tricky, due to the way magnesium behaves from a biochemical standpoint. Here’s a few of the most common testing methods:
RBC (Red Blood Cell) test: the accuracy of this test is somewhat debatable, since red blood cells don’t have mitochondria, which is where magnesium goes to work. Reliable ranges are between 4.2 and 6.8 mg/Dl, but these ranges have been recently adjusted to 3.5 to 6 mg/Dl to reflect the curve of the population the lab serves - read: levels are so low that the average has been lowered. If you do choose this method, remember you want to be above the 80th percentile, or above 6.0 - 6.5 mg/Dl for optimal health. If your doctor does not provide this test you can find a testing lab online at https://requestatest.com/
Conventional medicine is still using the Serum (blood) magnesium test, which is inaccurate to a significant degree because only 1% of all the magnesium in the body circulates in the blood. The active magnesium in body tissues and organs is ionized magnesium, which is only tested in research settings. Furthermore, under the stress of some health ailments the body will pump magnesium out of the cells and into the blood, giving false readings. This test is used in clinical settings, and its false ‘positives’ explain why magnesium deficiencies are still exceedingly underdiagnosed.
The Buccal Cell Smear Test (Exa Test) which is performed by collecting a sample of tissue cells by scraping them from under the tongue. This test provides an accurate measure of how much magnesium is in heart and muscle tissues, and it is covered by insurance.
Testing for calcium
A calcium test is usually part of a complete blood panel, with ranges as follows:
Total (both free and bound to albumin) blood calcium: 8.5 to 10.5 milligrams per deciliter (mg/dL)
Ionized (free) calcium: 4.65 to 5.2 mg/dl
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*My article, “Preventing cardiovascular disease: a nutrition design”, outlines a comprehensive nutrition approach for these conditions.
References:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5877920/
https://www.spandidos-publications.com/10.3892/mmr.2015.3930
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5620030/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6627343/
https://www.sciencedirect.com/science/article/pii/S2213231719309589
https://medlineplus.gov/lab-tests/mthfr-mutation-test/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3262611/
https://openheart.bmj.com/content/1/1/e000167