Cardiovascular Support

About 610,000 people die of heart disease in the U.S. every year — 1 in every 4 deaths.[1]

Heart disease is the leading cause of death for both men and women. More than half of the deaths due to heart disease in 2009 were in men.[1]

(CHD) is the most common type of heart disease, killing over 370,000 people annually.[1]

Every year, about 735,000 Americans have a heart attack. Of these, 525,000 are a first heart attack and 210,000 happen in people who have already had a heart attack.[2]

In a 2005 survey, most respondents — 92% — recognized chest pain as a symptom of a heart attack. Only 27% were aware of all major symptoms and knew to call 9-1-1 when someone was having a heart attack. [3] About 47% of sudden cardiac deaths occur outside a hospital. This suggests that many people with heart disease don’t act on early warning signs.[4]

Heart attacks have several major warning signs and symptoms:

• Chest pain or discomfort
• Upper body pain or discomfort in the arms, back, neck, jaw, or upper stomach
• Shortness of breath
• Nausea, lightheadedness or cold sweats [5]

Figure 1 shows the leading causes of death in the U.S. and for women.

Exercise, optimal nutrition with fruits and vegetables, and moderate alcoholic and smoking cessation reduce the risk of myocardial infarction by 80%. [6]

Research from the Atherosclerosis Risk in Communities (ARIC) Study has found that almost half (45%) of heart attacks appear to be clinically silent — that is, not associated with any symptoms at all, at least that the patient can recall. These sorts of silent heart attacks were picked up by use of a routine electrocardiogram (ECG). And these silent heart attacks weren’t just a meaningless abnormality picked up on a test. The silent heart attacks were associated with a similar risk of subsequent death as clinically detected heart attacks. [7.]

“The traditional evaluation, prevention and treatment strategies for the TOP FIVE CHD risk factors still result in a CHD gap. This means that about 50% of patients still have CHD or MI despite ‘normal’ levels of these risk factors as presently defined in the medical literature. There are important details within each of these TOP FIVE risk factors that are not being measured by physicians and are thus ignored in the prevention and treatment of CHD.”[8,9,10]

Only 10-15% of patients with coronary heart disease lack any of the five conventional risk factors of hypertension, hyperlipidemia, diabetes, smoking and obesity.[11]

Most healthcare professionals still order the basic cholesterol panel as shown in Figure 2. That panel has been available since black and white television, but is it adequate to determine if someone is at risk for cardiac disease?

Cholesterol: What You Need To Know

Cholesterol is a minor player in heart disease.
Cholesterol levels are a poor predictor of heart disease.
Half the people with heart disease have normal cholesterol.
Half the people with elevated cholesterol have healthy hearts.
Lowering cholesterol has extremely limited benefits. *

Current research has determined that the risk of an individual developing heart disease is more accurately determined by advanced lipid testing such as shown in Figure 4.

But this extensive testing takes longer to explain to patients, and it requires a more extensive knowledge of lipid metabolism and greater knowledge of biochemistry.

The theory that fat and cholesterol cause heart disease became widely accepted despite much evidence to the contrary. This evidence needs to be reexamined. The case needs to be reopened.

Many doctors did not agree with the cholesterol myth and questioned the science on which it was based. The studies upon which the cholesterol myth was based were later found to be problematic. The adoption of the cholesterol myth by mainstream organizations and the government had a strong political component to it. *

Cholesterol is the parent molecule for sex hormones (estrogen, progesterone and testosterone) as well as Vitamin D and bile acids needed for digestion. The only time cholesterol is a problem is if it’s oxidized (damaged), as it then sticks to the lining of the arteries and begins the process of inflammation.

The true cause of heart disease is inflammation.

Inflammation is initiated by damage from free radicals (oxidative stress).

The concept of “good” and “bad” is outdated.

Cholesterol Basics

Cholesterol is a waxy substance — technically a sterol — that is an important constituent of cell membranes. The vast majority of cholesterol is made in the liver, while the rest is absorbed from the diet.

Cholesterol is the basic raw material that your body uses to make Vitamin D; sex hormones such as estrogen, progesterone, and testosterone; and bile acids needed for digestion. Cholesterol travels in particles called lipoproteins, the most common of which are the high-density lipoproteins (HDL) and the low-density lipoproteins (LDL). *

What is HDL?

Old School

HDL is considered “good” cholesterol because it helps remove so-called “bad” cholesterol, LDL. When measured, HDL levels should be as high as possible, probably 60 milligrams per deciliter of blood (mg/dl) and above. Maintaining a healthy weight, physical activity, and a diet that includes healthy fat like olive oil are believed to keep HDL levels high.
New School

HDL is much more tightly controlled by genetics than LDL. A 2011 study from the National Institutes of Health, AIM-HIGH, found that HDL did nothing to protect against heart attacks, strokes or death.

It also noted that all HDL is not the same; HDL-2 particles are large and buoyant and the most protective, while HDL-3 particles are small and dense and may be inflammatory.

HDL-2 is anti-inflammatory and anti-atherogenic (atherosclerosis being a condition in which an artery wall thickens from accumulation of fatty materials, called plaque, induced by inflammation, inhibiting blood flow from the heart).

HDL-3, on the other hand, is poorly understood.

You want to have higher levels of HDL-2 than HDL-3.

The “new school” generally agrees that higher levels of HDL are desirable, but research is concentrating on the function of HDL subtypes rather than the total amount. Daniel Rader, M.D., director of preventive cardiology at the University of Pennsylvania, wrote in the New England Journal of Medicine, “Recent scientific studies have directed increasing interest toward the concept that the measure of the function of HDL, rather than simply its level in the blood, might be more important to assessing cardiovascular risk and evaluating new HDL-targeting therapies.”*

People may also have excess HDL that becomes dysfunctional and damages the arteries, as noted in Figure 6. CHD is coronary disease, metabolic syndrome is prediabetes and DM is diabetes. There are many conditions that may cause HDL to become dysfunctional, so a high HDL is not necessarily a good thing.

There are a number of clinical clues that can cause a healthcare provider to suspect dysfunctional HDL is present are listed in Figure 7.

What is APO-A-1?

HDL cholesterol is a fat and will not dissolve in blood. It must be carried through the blood attached to a protein carrier, called APO-A-1.

What is LDL?

Old School

LDL is “bad” cholesterol because it can build up in the arteries, impeding blood flow. Its level should be kept low.

Current standards are 100 to 129 mg/dl, with lower than 100 being the target for people for those at risk for heart disease and lower than 70 being the target for people at very high risk.

Too much saturated fat in the diet, inactivity and being overweight are considered to raise LDL levels. *

The limitations of LDL in predicting CHD are noted in Figure 8.

New School

All LDL is not the same. LDL-A is a buoyant, fluffy molecule that does no harm whatsoever as long as it is not damaged by oxidation (a process caused by free radicals that enables cholesterol to form plaque). LDL-B is a small, hard, dense, molecule that promotes atherosclerosis.

A pattern of high LDL-A is the most beneficial. Blood tests today are able to measure the number of LDL-A and LDL-B particles in a blood sample.

It is not the LDL that causes arterial plaque formation; it is the total number of particles and the size of the particles within the LDL molecule. The LDL-B particles are referred to as the small dense LDL, sdLDL.

As the total number of particles (LDL-P) increases, especially the type B (sdLDL), plaque formation increases. See Figure 9.

In Figure 10, four people all have the same LDL cholesterol, but as the total particle number increases, the risk of heart disease rises.

A person may have an elevated total LDL, but if the total particle number is normal, the death rate is 10%. In contrast, another person may have a low total LDL, but if total particle is elevated, the death rate is 20%.

Several published articles have demonstrated that determining the total particle number and size is more accurate in determining the risk of cardiovascular disease than LDL. By the way, statin drugs — popularly prescribed for those with high LDL cholesterol — are not effective in lowering particle number.

What is APO-B?

The various types of LDL cholesterol are fat and will not dissolve in blood. They must be carried through the blood attached to a protein carrier, called APO-B. See Figure 11. Attached to APO-B are all the so-called “bad cholesterol”: LDL, VLDL, IDL and Lp(a), so it is a summary of all the potentially harmful cholesterol particles.

What Is Lp(a)?

The most important cholesterol of all, which conventional tests do not focus on, is Lp(a), a very small, highly inflammatory particle that is thrombogenic (blood clotting). Dr. Sinatra calls it “the alpha wolf” of cholesterol particles.

In a healthy body, low Lp(a) levels aren’t much of a problem. Lp(a) circulates and carries out repair and restoration work on damaged blood vessels. However, the more repairs needed on arteries, the more Lp(a) is utilized; it concentrates at the site of damage, binds with a couple of amino acids within the wall of a damaged blood vessel, dumps it LDL cargo, and starts to promote the deposition of LDL into the wall, leading to more inflammation and ultimately to plaque.

Also Lp(a) promotes the formation of blood clots on top of the newly formed plaque, which narrows the blood vessel  further.

Lp(a) levels are genetically determined and are increased by estrogen depletion, hypercholesterolemia, severe hypothyroidism, uncontrolled diabetes, renal failure and nephrotic syndrome (a kidney disorder characterized by protein loss, swelling, and elevated blood cholesterol and lipoproteins).

The research data in Figure 12 indicates that Lp(a) is increased by statin drugs (Lipitor, Crestor).

Dietary Advice

Old School

Eat less than 300 mg of cholesterol a day and eat less that 10 percent of calories as saturated fat.

New School

According to the Framingham Heart Study, people who consumed the most cholesterol in their diets did not have any higher blood cholesterol levels than those who consumed the least amount. The effect of dietary cholesterol and blood (serum) is variable and individual, and for most people — though not all — the effect of dietary cholesterol and serum cholesterol is insignificant. See Figure 13.

In any case, because cholesterol is not as an important risk factor for heart disease as once thought, it doesn’t matter very much. Saturated fat raises cholesterol, but it raises overall HDL cholesterol and the good part of LDL cholesterol (LDL-A) far more than it raises the bad part of LDL cholesterol (LDL-B).

There is no evidence that supports a direct relationship between saturated fat and heart disease. *

As noted in Figure 14, if you substitute a saturated fat with a refined carbohydrate, coronary heart disease is increased.

Saturated Fat: What You Need To Know

Saturated fat has been wrongly demonized.

Saturated fat raises the “good” (HDL) cholesterol.

Saturated fat tends to change the pattern of your “bad” cholesterol to the more favorable pattern A (big, fluffy particles).

Several recent studies have shown that saturated fat is not associated with a greater risk of heart disease.

One study from Harvard concluded that, “greater fat intake is associated with less progression of coronary atherosclerosis, whereas carbohydrate intake is associated with a greater progression.”

In the Nurses’ Health Study, refined carbohydrates were independently shown to be associated with an increased risk for coronary heart disease.

Omega-6 fats, e.g., vegetable oils, are pro-inflammatory.

The balance between omega-6 and omega-3 is far more important than saturated fat intake is.

Low-fat diets work because they reduce omega-6 fats, not because they reduce saturated fats. *

Sugar: What You Need To Know

Hypertension, high levels of triglycerides and a high ratio of triglycerides to HDL are all better predictors of heart disease then cholesterol. Sugar, or more specifically, fructose, raises every single one of these components; it’s the number one dietary contributor to heart disease, a far greater danger to your heart than fat — and the missing link among diabetes, obesity, and heart disease.

Fat raises LDL cholesterol, but it does so via big fluffy, harmless particles (producing the desirable pattern A profile) and lowers the nasty little BB gun-pellet LDLs that actually do cause heart disease. Sugar, in contrast, has the opposite effect, increasing the number of really bad LDL molecules (producing the harmful pattern B profile) and decreasing the number of harmless ones.

One top of that, high levels of sugar and insulin damage those nasty little LDL particles, making them far more likely to start the process of inflammation.

If you accept the theory that inflammation, not cholesterol, is at the “heart” of heart disease, it’s worth pointing out that the metabolic effects of sugar are highly inflammatory to your artery walls.

Also be aware that:

1. High sugar intake drives up the hormone insulin, which raises blood pressure and increases cholesterol.
2. When sugar in the bloodstream sticks to proteins, it creates damaging and toxic molecules called advanced glycation end products, or AGEs. The same process also damages LDL, contributing to inflammation and ultimately to heart disease. *

Statin Drugs: What You Need To Know

The benefits of statin drugs have been widely exaggerated, and are nothing to do with their ability to lower cholesterol. Statin drugs deplete coenzyme Q10, one of the most important nutrients in the heart, and that can cause muscle pain, weakness and fatigue.

The brain depends on cholesterol to function optimally.

Cholesterol helps stimulate thinking and memory.

Statin drugs lead to a reduction in sex hormones, as shown by several studies. Sexual dysfunction is a common (but under-reported) side effect of statin drugs.

Statins interfere with serotonin receptors in the brain.

There are troubling indicators that statin drugs may be associated with a higher risk for cancer and diabetes.

A comprehensive study by the University of California San Diego School of Medicine showed that a majority of doctors dismiss complaints of side effects from statins and do not report them to Medwatch, the FDA’s system for reporting any undesirable experiences associated with the use of medical products or drugs. In other words, statins’ side effects are grossly under-reported.  *

The following laboratory information was obtained from Boston Heart.com and Cleveland Heart.com. All these laboratory values are markers for heart disease and should be obtained in anyone being evaluated for possible heart disease, along with a complete history and physical, EKG, echocardiogram, stress test and cardiac cauterization if indicated.

Adiponectin

Adiponectin is a measure of the amount of a hormone produced by fat cells that protects against developing heart disease and diabetes.

Lab Values 

Male:

Optimal: >10.0 µg/dL
Borderline: 7.0-10.0 µg /dL
High risk: <7.0 µg/dL

Female:

Optimal: >13.0 µg/dL
Borderline: 9.0-13.0 µg /dL
High risk: <9.0 µg/dL

Clinical Significance: Low values indicate increased risk of diabetes

Glycated Serum Protein (GSP)

GSP is the amount of glucose attached to total serum proteins that indicates the average amount of glucose in the blood over the previous two to three weeks.

Lab Values
Optimal: <200 µmol/L
Borderline: 200-250 µmol/L
High risk: >250 µmol/L

Clinical Significance: Borderline or high values indicate increased risk of diabetes

Glucose

Glucose, the major short-term source of energy for the body, is obtained from the diet and produced in the liver.

Lab Values
Normal:  70-99 mg/dL
Borderline: 100 – 125 mg/dL
High: > 126 mg/dL, classified as diabetes mellitus
Critical values: <30, >600 mg/dL

Clinical Significance: A fasting glucose level of ≥ 126 mg/dL indicates the presence of diabetes mellitus, associated with a significantly increased risk of developing CVD, stroke, peripheral vascular disease, kidney failure, neuropathy and retinopathy. The presence of diabetes mellitus needs to be confirmed by also having an elevated HbA1c level. A value < 30 mg/dL indicates significant hypoglycemia.

Hemoglobin A1C (HbA1c)

This test measures the concentration of glucose attached to the hemoglobin in red blood cells. It assesses the average amount of glucose in blood over the last two to three months.

Lab Values
Optimal: <5.7%
Borderline: 5.7–6.4%\
High risk: >6.4%
Alert: >11.9 %

Clinical Significance: Monitors efficacy of diabetes treatment over time and identifies patients at risk of developing diabetes

Insulin

Insulin is a hormone responsible for the transportation and storage of glucose in cells. It regulates glucose levels in blood. This test measures the amount of insulin in blood.

Lab Values
Low: <5 µU/mL (normal in a non-diabetic, but low if the patient has diabetes [consistent with type 1 diabetes])
Optimal: 5 µU/mL
High: >5 µU/mL

Clinical Significance: Insulin may be used in conjunction with glucose or glucose tolerance tests to:

• Diagnose insulin resistance
• Diagnose insuloma
• Monitor the amount of endogenous insulin production
• Determine when a type 2 diabetic may need to start insulin therapy

Insulin Resistance

The standard measure of insulin resistance is the homeostasis model, based on both fasting insulin and fasting glucose level.

Lab Values
Optimal:  <2.0
Borderline: 2.0 – 3.0
High Risk: >3.0

Clinical Significance: The presence of insulin resistance (value > 3.0) indicates a high risk of developing:

• Coronary heart disease
• Stroke
• Peripheral vascular disease
• Type 2 diabetes mellitus
• Hypertension
• Hyperlipidemia

Fibrinogen

Fibrinogen or Factor I, an acute phase inflammatory plasma protein synthesized by the liver, is an essential component in the clotting cascade.

Lab Values
Optimal: <370 mg/dL
Borderline: 370-470 mg/dL
High risk: >470 mg/dL

Clinical Significance: Fibrinogen is converted by thrombin to form fibrin. Fibrin is then cross-linked by factor XIII, and is the final step in the formation of a blood clot. Elevated levels are associated with inflammation. Every 100 mg/dL increase in plasma fibrinogen level > 370 mg/dL has been associated with a 1.8-fold increased risk of CVD.

High Sensitivity C-Reactive Protein (hs-CRP)

CRP is a protein produced in the liver in response to systemic inflammation and is an acute phase reactant. The “high sensitivity” CRP test is needed to detect very low levels of CRP, which may be seen with vascular and/or systemic inflammation.

Lab Values
Optimal: <1.0 mg/L
Borderline: 1.0–3.0 mg/L
High risk: >3.0 mg/L

Clinical Significance: An independent predictor of developing CVD events that provides independent prognostic information after initiating treatment.

Lipoprotein-Associated Phospholipase A2 [LpPLA2] (PLAC Assay)

LpPLA2 is an enzyme produced by monocytes/macrophages that breaks down phospholipids. Increased blood levels are associated with increased atherosclerosis.
Lab Values
Optimal:  <200 ng/mL
Borderline: 200–235 ng/mL
High risk: >235 ng/mL
Clinical Significance: Predicts CVD risk independent of LDL-C and other inflammatory markers. Associated with:

• 2-fold increased risk for coronary events
• 2-fold increased risk for stroke
• 11-fold increased stroke risk if CRP is also elevated

Myeloperoxidase (MPO)

This is an enzyme made by white blood cells in the artery wall. Elevated levels of MPO indicate the presence of unstable plaque or buildup in the arterial wall and a high risk of having a near-term cardiovascular event (within one to six months). In patients with high levels of MPO, healthcare professionals should carefully evaluate CVD risk.

Lab Values
Optimal: <350 pmol/L
Borderline: 350-633 pmol/L
High risk: >633 pmol/L
Alert: >1658 pmol/L

Clinical Significance: Elevated MPO levels (>633 pmol/L) have been shown to be a significant independent risk factor for a major adverse cardiac event (MACE) over the ensuing one to six months in patients presenting with chest pain who have normal levels of troponin. This is especially the case if levels of high sensitivity C- reactive protein (hs-CRP) are also elevated (>2 mg/L), along with increased (>235 ng/mL) lipoprotein associated phospholipase A2 (LpPLA2).

Elevated serum levels of CRP are a marker of generalized inflammation. Levels of LpPLA2 greater than 2 are markers of inflammation in the arterial wall. Simultaneous elevated levels of MPO (>633 pmol/L), hs-CRP (>2.0 mg/L) and LpPLA2 (>235 ng/mL) are associated with markedly increased six-month risk of a MACE.

Figure 15 shows how the markers noted above may be used to determine the degree of plaque formation.

Triglycerides

Triglycerides are a type of fat (lipid) found in your blood. When you eat, your body converts any calories it doesn’t need to use right away into triglycerides. The triglycerides are stored in your fat cells. Later, hormones release triglycerides for energy between meals. If you regularly eat more calories than you burn, particularly “easy” calories like carbohydrates and fats, you may have high triglycerides (hypertriglyceridemia).

Lab Values

Normal — Less than 150 milligrams per deciliter (mg/dL), or less than 1.7 millimoles per liter (mmol/L)
Borderline high — 150 to 199 mg/dL (1.8 to 2.2 mmol/L)
High — 200 to 499 mg/dL (2.3 to 5.6 mmol/L)
Very high — 500 mg/dL or above (5.7 mmol/L or above)

Clinical Significance: Elevated triglycerides are associated with an increased risk of heart disease.

Homocysteine

Homocysteine is an amino acid produced by ineffective protein metabolism that promotes free radical production.

Lab Values

Optimal values: 7 or less µmol/L

Clinical Significance: Increased levels elevate triglycerides and cholesterol synthesis. Increased risk of stroke by 42%, peripheral vascular disease by 28% and heart attacks by 30%. Individuals with a history of hypertension and elevated homocysteine levels are 25 times more likely to die from a heart attack or stroke.

MTHFR Genotype Test

MTHFR (methylenetetrahydrofolate reductase) is the enzyme responsible for metabolizing folate, which is essential for converting homocysteine to methionine. Homocysteine is a necessary amino acid that plays an important role in metabolism, but high levels are related to a higher risk of coronary heart disease, stroke and peripheral vascular disease. The intended use of MTHFR genetic testing is, along with assessing homocysteine levels, to assess and minimize a patient’s risk for CVD through nutritional therapy and possibly clot prevention with low dose aspirin

Lab Values

Genotypes:
677C/C   1298A/A; 677C/T   1298A/A; 677T/T   1298A/A
677C/C   1298A/C; 677C/T   1298A/C;  677T/T   1298A/C
677C/C   1298C/C;  677C/T   1298C/C;  677T/T   1298C/C
Clinical Significance:
677(C/C) genotype – normal folate metabolism; 1298(A/A) genotype – no variant
677(C/T) genotype – single copy of variant; 1298(A/A) genotype – no variant
677(T/T) genotype – significant variant associated with reduced folate        metabolism; 1298(A/A) genotype – no variant
677(C/C) genotype – no variant; 1298(A/C) genotype – single copy of variant
677(C/T) genotype – single copy of variant; 1298(A/C) genotype – single copy of variant
677(T/T) genotype – significant variant associated with reduced folate metabolism; 1298(A/C) genotype – single copy of variant
677(C/C) genotype – no variant; 1298(C/C) genotype – two copies of variant
677(C/T) genotype – single copy of variant; 1298(C/C) genotype – two copies of variant
677(T/T) genotype – significant variant associated with reduced folate metabolism; 1298(C/C) genotype – two copies of variant

Apolipoprotein E (apoE) Genotype Test

ApoE is a critical protein component of very low-density lipoprotein (VLDL) and chylomicrons. ApoE is important for cholesterol absorption from the intestine and uptake of triglyceride-rich lipoproteins  by the liver.

The intended use of ApoE genetic testing is to aid in the selection of optimal cholesterol-lowering protocols by healthcare providers. The genetic test identifies individuals with altered lipid transport. Depending on the apoE genotype, cholesterol-lowering dietary interventions may be very effective in these individuals, so determination of the genotype allows physicians to select the most efficacious treatment regimen for patients for lowering low density lipoprotein cholesterol and reducing heart disease risk.

The apoE gene has three common alleles (e2, e3, e4) that encode for three protein isoforms (E2, E3, E4). ApoE3 is the most common form of apoE. Population frequencies for these apoE alleles are:

e2 (15%)
e3 (65%)
e4 (20%)

N-Terminal Pro-Brain Natriuretic Peptide (NT-proBNP)

Brain natriuretic peptide (BNP) is a neurohormone that affects body fluid homeostasis via diuresis and natriuresis. Elevated levels are seen in patients with congestive heart failure, and a decreased ejection fraction. NT-proBNP is the precursor molecule for BNP
Lab Values

Age: ≤75 yrs.
Optimal: <125 pg. /mL
Borderline: 125–450 pg. /mL
High risk: >450 pg. /mL

Age: >75 yrs.
Optimal: <450 pg. /mL
High risk: >450 pg. /mL

Clinical Significance: Elevated levels Identify subjects with left ventricular dysfunction. Every incremental increase in values above normal is associated with an incremental increase in CV risk. Levels >450 pg. /mL in subjects with stable CAD are associated with a 2- to 6-fold increased risk for cardiac morbidity and/or mortality. Normal levels exclude cardiac dysfunction.

Trimethylamine N-oxide (TMAO)

Gut microbes live symbiotically within the human digestive tract and play important roles in host defense, immunity, and nutrient processing and absorption. This diverse community is unique to each person and influenced by acute and chronic dietary exposures to various food sources.

Nutrients such as phosphatidylcholine (also known as lecithin), choline, and L-carnitine are abundant in animal-derived products such as red meat, egg yolk, and full-fat dairy products. When consumed, these nutrients are processed by gut bacteria, resulting in the release of various metabolites, including TMA (trimethylamine), into the blood. TMA is then transported to the liver, where it is converted into TMAO (trimethylamine N-oxide), which has been shown to regulate various physiological processes involved in the development of atherosclerosis.i

Clinical Significance: There is a dose-response relationship between TMAO and atherosclerotic burden in individuals undergoing elective diagnostic coronary angiography. In stable individuals undergoing elective cardiac evaluation, elevated TMAO levels are associated with increased risk of cardiovascular disease, or major adverse cardiovascular events (MACE: MI, stroke or death) at a 3-year follow-up.

Plasma L-Carnitine (a dietary precursor to TMAO) is also associated with increased risk of cardiovascular disease and MACE, but only in individuals with simultaneously elevated TMAO levels. In a “low risk” subset of the aforementioned population, people with optimal LDL-C 70mg/dL or apoB <80mg/dL), but elevated TMAO, were just as likely to experience a major adverse cardiovascular event.

Lab Values ((μM)
<6.2 Low
6.2-9.9 Moderate
≥10.0 High

The following are suggestions from Mark Houston, M.D., from his article, “The Role of Nutraceutical Supplements in the Treatment of Dyslipidemia.”12 Also see Figure 16.

Inhibition of LDL oxidation

Niacin
Green tea extract and green tea
Pantethine
Monounsaturated fats
Curumin
Pomegranate
Garlic
Sesame
Gamma ⁄ delta tocotrienols
Lycopene
Polyphenols
Oleic acid
Glutathione
Citrus bergamot
Policosanol

Inhibition of low-density lipoprotein glycation

Carnosine
Histidine
Myricetin
Kaempferol
Rutin
Morin
Pomegranate
Organosulfur compounds

Lower low-density lipoprotein
Niacin
Red yeast rice
Plant sterols
Sesame
Tocotrienols (gamma ⁄ delta)
Pantethine
Citrus bergamot
Green tea extract and green tea
Omega 3 fatty acids
Flax seed
Monounsaturated fats
Garlic
Resveratrol
Curcumin
Orange juice
Soluble fiber
Krill oil
Convert dense low-density lipoprotein B to large low-density lipoprotein A
Niacin
Omega 3 fatty acids
Plant sterols

Reduce intestinal cholesterol absorption
Plant sterols
Soy
Green tea extract and green tea
Flax seeds
Sesame
Garlic
Fiber

HMG CoA reductase inhibition (decrease cholesterol production)
Red yeast rice
Pantethine
Gamma ⁄ tocotrienols
Sesame
Green tea extract and green tea
Omega 3 fatty acids
Citrus bergamot
Garlic
Curcumin
Gamma-linolenic acid
Plant sterols

Lower lipoprotein(a)
Niacin
N acetyl cysteine
Gamma delta tocotrienols
Omega 3 fatty acids
Flax seed
Coenzyme Q10
Vitamin C
L Carnitine
L-Lysine
L-Arginine

Lower triglycerides
Niacin
Red yeast rice
Omega 3 fatty acids
Pantethine
Citrus bergamot
Flax seed
Monounsaturated fats
Resveratrol
Orange juice
Krill oil

Increase total high-density lipoprotein (HDL) and HDL 2b levels and convert HDL 3 to HDL 2 and 2b
Niacin
Omega 3 fatty acids
Pantethine
Red yeast rice
Monounsaturated fats
Resveratrol
Curcumin
Pomegranate
Orange juice
Citrus bergamot
Krill oil

Reduce inflammation
Niacin
Omega 3 fatty acids
Flax seed
Monounsaturated fats
Plant sterols
Guggulipids
Resveratrol
Glutathione
Lower apolipoprotein B lipoprotein
Increase apolipoprotein A1 lipoprotein
Decrease low-density lipoprotein particle number
Lower apolipoprotein B lipoprotein
Niacin
Omega 3 fatty acids
Plant sterols
Green tea extract and green tea

Increase apolipoprotein A1 lipoprotein
Niacin

Decrease low-density lipoprotein particle number
Niacin
Omega 3 fatty acids

Nutraceutical Supplement Recommended Doses For The Treatment Of Dyslipidemia

Recommended Supplements to Address Cardiovascular Health:

References

1. Coronary heart disease (http://www.cdc.gov/heartdisease/coronary_ad.htm)
2. heart attack (http://www.cdc.gov/heartdisease/heart_attack.htm)
3. CDC, NCHS. Underlying Cause of Death 1999-2013 on CDC WONDER Online Database, released 2015. Data are from the Multiple Cause of Death Files, 1999-2013, as compiled from data provided by the 57 vital statistics jurisdictions through the Vital Statistics Cooperative Program. Accessed Feb. 3, 2015.
4. Mozaffarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics—2015 update: a report from the American Heart Association. Circulation. 2015; 131:e29-322.
5. CDC. State Specific Mortality from Sudden Cardiac Death: United States, 1999(http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5106a3.htm). MMWR. 2002;51(6):123–126.
6. Lancet 2004; 364:937
7. (Am J Epidemiol. 1989 Apr;129(4):687-702)
8. Journal of the American Society of Hypertension 2010;4:272
9. Circulation 2007;115:1020 ,Expert Rev in CV Therapy 2010;8:821
10. Nephrol Dial Transplant 2006:21:850
11. (JAMA 2003;290:898 JAMA 2003;290:891)
12. J Clin Hypertens (Greenwich). 2012;14:121–132.

* The Great Cholesterol Myth by Jonny Bowden, Ph.D., C.N.S & Stephen Sinatra M.D., F.A.C.C.