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Nutrients for Heart Health: An Integrative Approach to Cardiovascular Health

An interview with Daniel Chong, ND Daniel Chong, ND, takes an integrative approach to cardiovascular health. He has been in private practice since 2000, and has completed additional training in cardiometabolic medicine from the American Academy of Anti-Aging Medicine. He’s also a contributing editor in cardiology for the Natural Medicine Journal and a consultant for Boston Heart Diagnostics Lab. Dr. Chong serves patients in a traditional practice setting and through online consults. https://www.emersonecologics.com/blog/post/integratie-cardiovascular-health


In this interview with Element Senior Writer Sarah Cook, ND, Dr. Daniel Chong shares insights into the intimate connections between nutrients and cardiovascular health.

SARAH COOK: Before we dive into nutrients, can you give a quick refresher on the mechanisms of heart disease?

DANIEL CHONG: Sure. Let’s start with the conventional view of how heart disease develops.

I want to be clear that I don’t consider this conventional view wrong or inaccurate. The steps involved in the development of cardiovascular disease are well accepted. Integrative explanations for heart disease don’t dispute the conventional paradigm but, instead, add to it.

So, here are the steps:

Technically speaking, cardiovascular disease is preceded by one or more ongoing insults to the vascular wall, in combination with some degree of susceptibility, often due to genetic predisposition, nutritional inadequacy, and other risk factors. The traditional risk factors that are accepted in the conventional paradigm are smoking, hypertension, hypercholesterolemia, diabetes, and obesity, with chronic inflammation also emerging as another accepted risk factor.


These traditional risk factors also apply to the viewpoint I take but from a slightly different perspective.

Persistence of this combination of factors over time leads to endothelial dysfunction. There is no anatomical change at this point; just a functional change. Endothelial dysfunction and resulting damage to the endothelium leads to increased vulnerability to low-density lipoprotein (LDL) and other particles penetrating the vascular wall.

When these particles get stuck in the arterial wall and other factors like oxidative stress are also present, the protein structures can change and essentially become viewed as foreign particles. An immune response follows, with foam cells, fatty streaking, and eventual plaque formation, or atherosclerosis.

A majority of cardiovascular events are caused when an atherosclerotic plaque ruptures and a local thrombus forms. A common misconception is that heart attacks occur when a plaque simply grows large enough to block a coronary artery. But more often, a heart attack occurs when a smaller, inflamed, and weak plaque ruptures. Again, the ruptured plaque causes thrombosis and, if severe enough, myocardial infarction.

There is no arguing that these steps define the pathogenesis of cardiovascular disease. Where certain integrative approaches differ from the conventional is in asking why this occurs and how the answers can help guide how we want to approach it.

COOK: Tell me more about this approach to cardiovascular disease.

CHONG: The perspective I have learned differs from the conventional approach because it views the process of atherosclerosis as purposeful, versus purely pathologic. In fact, in some ways it can even be viewed from the perspective of a necessary, though backup, repair process.

Imagine if the body didn’t repair a weakened and damaged endothelium. Over time, this damage would worsen and the arterial wall could rupture, creating a hemorrhage and, if in a large enough vessel, rapid death. Recent research findings suggest that plaque formation may actually occur as a protective mechanism to help prevent a person from such an untimely death. A potential explanation is that this is an adapted mechanism that can allow a person to live long enough to reproduce and thus help propagate the species, before finally succumbing to the effects of this back up mechanism. With the primary goal of a species in nature being species propagation, this would make sense.

So when there is repeated damage to the wall of the blood vessel which the body cannot control for various potential reasons, the body mobilizes this repair process, similarly to other types of healing responses. Cholesterol is obviously crucial to cell wall integrity and any repair process. Other nutrients are also needed. The thinking here would be that LDL and other atherogenic particles may actually carry cholesterol and these nutrients to the site of damage.

If these particles and the immune reaction to them accumulate, eventually a plaque is formed. The body then tries to stabilize and calcify that plaque. Typically it is ongoing inflammation and oxidative stress that can make a plaque become vulnerable to rupture. Nutrient inadequacies have a lot to do with the progression as well as the etiology of cardiovascular disease.

“Nutrients that support collagen production include vitamin C, proline, lysine, copper, zinc, manganese, and vitamin A. Although all of these nutrients are required for collagen production, they will not fulfill this function without adequate vitamin C. ”


COOK: Can you expand on the role nutrient inadequacies play in cardiovascular disease?

CHONG: Nutrient inadequacy may be a key starting point that makes blood vessels more vulnerable to endothelial dysfunction and damage in the first place. The conventional paradigm considers genetics and traditional risk factors as the major contributors, but if a person is nutritionally replete, the vascular endothelium will function better and thus they may be less susceptible to these traditional risk factors.

Here’s how I explain the process:

Nutrient inadequacies contribute to endothelial dysfunction, smooth-muscle dysfunction, and/or weakened collagen. Blood vessels then become weak and vulnerable to structural damage—particularly at sites where hemodynamic forces create more stress on arterial walls. This is why plaques mostly form at areas where there is high turbulence or shear stress.

Then, to prevent hemorrhage, the repair process mobilizes. Fat and nutrient transporters enter the endothelial wall. Immune activation leads to structural repair via plaque formation and stabilization.

This perspective of cardiovascular disease progression would suggest this process is not random or fatalistic. In this model, it serves the biological purpose of extending lifespan. Also, the idea that nutrient inadequacies may precede and contribute to the pathogenesis empowers people. Nutrition is modifiable and gives people control over their health.

COOK: What nutrients do you recommend to support cardiovascular health?

CHONG: I recommend nutrients that are required to support three main functions: endothelial function, smooth-muscle function, and collagen production. Let’s take a look at each.

Endothelial function refers to the ability of vascular endothelial cells to release substances that regulate vascular contraction and relaxation, blood clotting, immune function, and platelet adhesion. One thing that characterizes endothelial dysfunction is decreased production of vasodilating compounds, like nitric oxide (NO). It’s also characterized by increased production of proinflammatory and procoagulant compounds.


Nutrients to support endothelial function include those that support NO production, antioxidant activities, and healthy inflammatory pathways.

Production of NO relies on l-arginine as a precursor molecule, as well as B vitamins (B6, B12, and folic acid) as enzymatic cofactors. Dietary nitrates from vegetables also act as precursors for NO. Studies have shown that eating more green leafy vegetables correlates with healthy NO production.

Antioxidants that support endothelial function include vitamin C, vitamin E, coenzyme Q10 (CoQ10), and flavonoids.* Hawthorne is a nutritive herb that’s rich in flavonoids and other antioxidants to support cardiovascular health.* Essential fatty acids (EFAs) support healthy inflammatory pathways.* My preferred EFA source aside from food is algae oil.

Smooth-muscle function is needed for healthy vasoconstriction and vasodilation. It’s related to endothelial function because the endothelial cells release substances that influence smooth-muscle contraction and relaxation. That means that the same nutrients that support NO production, like l-arginine, can also support smooth-muscle function.* Other nutrients needed for smooth-muscle function include calcium, magnesium, and potassium.*

Collagen is the main protein in connective tissue throughout the body, and an essential component of blood vessels. Nutrients that support collagen production include vitamin C, proline, lysine, copper, zinc, manganese, and vitamin A. Although all of these nutrients are required for collagen production, they will not fulfill this function without adequate vitamin C.

COOK: Tell me more about the link between vitamin C and cardiovascular health.

CHONG: The idea that vitamin C may be a key component in cardiovascular health was first conceptualized by Linus Pauling and Matthias Rath around 1990. Humans are one of the few animals on the planet that are unable to make vitamin C. They are also one of the few animals that readily develop cardiovascular disease. Interestingly, the only lab animals that naturally and easily get heart attacks like we do are guinea pigs, and they don’t make vitamin C either.

It’s thought that pre humans produced an enzyme called L-gulonolactone, which was the rate-limiting factor for synthesizing vitamin C in the liver. It’s estimated that a few million years ago, a mutation occurred that turned the production of that enzyme off, and these pre humans lost the ability to manufacture vitamin C.

Interestingly, Vitamin C is required for collagen production. With collagen being crucial for strong blood vessels, Pauling and Rath suggested that vitamin C insufficiency weakens blood vessel walls and triggers the biological repair process that I described above (leading to plaque formation).


Their early models also suggested that one of the most effective “repair molecules” to be mobilized during the process was lipoprotein(a) [Lp(a)]. They hypothesized an inverse relationship between the production of Lp(a) and vitamin C levels, and proposed that Lp(a) might act as a surrogate to protect the blood vessels when vitamin C levels decline.

The Dr. Rath Research Institute then developed a mouse model to imitate human metabolism. The mice were genetically altered to lose the ability to produce vitamin C and at the same time gain the ability to produce Lp(a). Mice were placed on a consistent diet with varied amounts of vitamin C (in the form of ascorbic acid).

The study results showed that mice consuming less vitamin C produced more Lp(a). Also, the production of Lp(a) paralleled the development of atherogenic plaques. Even more exciting is that the researchers were able to achieve a level of vitamin C where the mice had no plaque formation at all.

COOK: How much vitamin C should people consume to support cardiovascular health?


CHONG: Technically, it is going to be highly individualized, but one way to try and answer this question is to look at vitamin C consumption of animals in the wild. Gorillas are similar to humans in that they cannot synthesize vitamin C. But gorillas don’t get cardiovascular disease in the wild. In their natural diet, gorillas can consume 4,000 mg or more of vitamin C per day.

We can also look at vitamin C production in animals that produce it endogenously. Goats are an excellent example because they’re similar in size to humans. Goats also produce a baseline amount of vitamin C in the few thousands of milligrams per day when they’re healthy and not under stress. Interestingly, when they are exposed to stress of any kind, they increase production of vitamin C to over 10,000.

I don’t feel many of the human studies of vitamin C supplementation have been useful in estimating the amount that’s sufficient to support cardiovascular health. One reason is that the studies that have looked at the relationship between vitamin C and heart health have rarely used supplementation with more than 1,000 mg per day. Many have not shown a beneficial effect, but that amount is much lower than the amounts we see animals producing or consuming in the wild, so it’s not necessarily surprising.

The amount of vitamin C that any person needs depends on their diet, lifestyle, level of stress, and overall health. We know that animals increase production of vitamin C when they have an infection or are exposed to stress. With poor diets and high stress being the norm in our society, it’s hard to say how much vitamin C the average patient needs, but clearly it’s well above the RDA. It’s also interesting to note that intestinal absorption of vitamin C increases under conditions of stress.

What I recommend to my patients is to eat a diet that’s rich in vitamin C. That means eating bountiful fruits and vegetables. But sometimes food is not enough. To support optimal vitamin C levels, I recommend some adults also supplement with about 2,000 mg per day. Some patients may need more, depending on their diet and lifestyle.

The best way to mimic nature is to consume these added doses of vitamin C at multiple intervals throughout the day. It’s better to take 500 mg three times a day than to take 1,500 mg at once. Vitamin C can be given in the form of ascorbic acid and combined with bioflavonoids for their synergistic and antioxidant effects.

COOK: In addition to nutrient inadequacies, what other lifestyle factors affect cardiovascular health?

CHONG: Several factors are known to contribute to endothelial dysfunction. These include smoking, exposure to environmental toxins, inflammatory responses, obstructive sleep apnea, diets high in sugar or refined carbohydrates, diets high in saturated fat or refined oils, stress, and physical inactivity.

There’s some interesting research on the frequency of movement throughout the day. If a person walks or runs for six minutes every hour for 10 hours a day, they have a better benefit than sitting for nine hours and then walking or running on the treadmill for one hour. Our bodies are not meant to be sedentary. Frequent movement is key.

The topic of diet in health can lead to heated debate amongst practitioners, and I would never say there is only one way to do things. However, I think it’s important to inform patients that the only diet that has been shown in research to actually reverse arterial plaque is a whole foods, plant-based diet as promoted by people like Dean Ornish and Caldwell Esselstyn. I recommend versions of this diet, but with the caveat that every patient is unique. I always monitor a patient’s response to dietary changes with biomarkers and imaging.

COOK: How important do you believe LDL cholesterol is as a cardiovascular biomarker?

CHONG: LDL is only part of the story. If elevated LDL, in and of itself, could singly explain atherosclerosis, we would have plaques forming on all of our arteries and veins. We don’t. Instead, plaque mostly forms in the coronary arteries and at other points where hemodynamic forces place more shear stress on arterial walls.

Also, if LDL particles were the sole cause of atherosclerosis, animals that have extremely high levels would suffer from severe cardiovascular disease. They don’t. It’s almost impossible to find an animal in a natural setting with heart disease. Brown bears in the wild have serum cholesterol levels that vary between 300 and 600 mg/dL. Yet there is no evidence that these bears develop plaques or have heart attacks at all.

To explain the relationship between LDL particles and cardiovascular health, I use the analogy of a chain link fence. The arterial wall is the fence. The LDL particles are like a bunch of tennis balls in a bucket. We can throw the tennis balls at the fence, and the ones that get through are like the LDL particles that get stuck in the arterial walls. We can decrease the chances of LDL getting through by either making the chain links smaller (e.g., supporting endothelial function, smooth-muscle function, and collagen production) but also by decreasing the number of tennis balls (e.g., lowering LDL).

In high-risk cases, we want to do both. We might use a statin medication to lower LDL, or a dietary supplement like red yeast rice to support healthy levels. For generally healthy patients, it makes the most sense to work on the chain link fence—with nutrients that support endothelial function, smooth-muscle function, and collagen production.

Remember that with Pauling and Rath’s theory, LDL can be considered a type of repair molecule that serves a purpose. When we replenish nutrients, there’s a lesser need for repair, and a natural consequence will be that LDL goes down. When we see this happen naturally, and all we’ve done is support nutrition and lifestyle, that’s a very good sign.

COOK: How important is homocysteine as a cardiovascular risk factor?

CHONG: There is some controversy about this. But regardless of whether or not it contributes to cardiovascular risk, there’s no question that homocysteine is a marker to consider in methylation. I run it in all of my patients for this reason alone.

Elevated homocysteine indicates impaired methylation and a higher potential need for vitamins B6, B12, and/or folate. These nutrients also support endothelial function.

COOK: What cardiovascular assessments do you routinely order?

CHONG: For routine screenings, I order advanced lipid testing in addition to a standard cholesterol profile. The panel typically includes LDL particle number (LDL-P), apolipoprotein B (apoB), apolipoprotein A1 (apoA1), and Lp(a). I also order homocysteine, C-reactive protein (CRP), hemoglobin A1C (HbA1C), fasting insulin, and vitamin D (25[OH]D) frequently.

For patients with a strong family history of cardiovascular disease or a high number of risk factors, I may also order trimethylamine-N-oxide (TMAO), asymmetric dimethyl arginine (ADMA), and imaging.

Imaging could be in the form of a carotid intima thickness test (CIMT) or electron-beam tomography (EBT) coronary artery calcium score.


Calcium scores are more valuable the older a patient is, whereas we see earlier and subtler changes in the CIMT.

COOK: What words of wisdom do you have for other practitioners supporting patients’ cardiovascular health?

CHONG: Sifting through the mass of opinions and recommendations related to cardiovascular health can be overwhelming. One piece of advice is to look for endpoint evidence of benefit. There are so many studies that measure outcomes like LDL, HDL, blood pressure, or weight loss.


These are important, but they don’t necessarily inform us whether an intervention affects the outcome of interest: plaque formation and cardiovascular events. If a study evaluates endpoint evidence, that’s an intervention you can better rely on.

And finally, trust your medicine and the body’s ability to heal. Newer clinicians I consult with often ask if they should refer a patient to a cardiologist. I respond with this question: What will the cardiologist do that you won’t? Sure, there are cases where a referral is certainly indicated.


But for cardiovascular risk reduction, integrative approaches offer more tools and flexibility than conventional protocols. There is good evidence that when we give the body what it needs (and remove what it doesn’t), the body will respond. As long as we are being thorough and assessing for positive change, we should trust our medicine. 


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