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Demystifying Heart Attacks: Their True Cause, How to Prevent Them and How Western Medicine Has Misled Us
On January 5, 2021, I found myself in the back of an ambulance and in the worst pain I have ever experienced. I was having a heart attack at the young age of thirty-four. I would later find out that it was a “widowmaker” heart attack, in which there is a 100 percent blockage of the left anterior descending (LAD) artery. Only 12 percent of people who have a widowmaker outside of a hospital setting survive.1 Fortunately, this is one situation where Western medicine is useful, and I made it to the hospital in time for them to save my life.
The research I have done to understand what happened that day has made me question everything medicine ever told me about heart disease and the cause of heart attacks. It has also made me wonder what particular part of what they did that day in the hospital was actually lifesaving. Further, it is clear that the medications and procedures that Western medicine uses to prevent heart attacks are not working and are one of the reasons why heart disease remains the number-one killer in the world. I detail my frustrating experience in the hospital, as well as many of my thoughts on heart disease, in my book, Understanding the Heart.
CHOLESTEROL: A BROKEN RECORD
While recovering in the hospital, I questioned the doctors about what they thought had caused my heart attack. The answer was the same whether I asked an attendant, resident, medical student or nurse—a broken record of “high cholesterol.” The image of the angiogram done in the hospital that day showed the blockage and what seemed to be less blood flowing into the branches of the artery downstream of the blockage (Figure 1).
At the time of the heart attack, my cholesterol was “high” and had been so for the three years prior. I was very aware of this. I am a type 1 diabetic, and eating a lower carbohydrate diet makes it very easy to control my blood sugar levels. In people who are metabolically healthy, eating a lower carbohydrate diet has been shown to create elevations in their LDL (the so-called “bad” cholesterol) and total cholesterol, but this “tends to occur in the context of otherwise low cardiometabolic risk.”2 Research indicates that long-term higher LDL in these individuals does not result in the development of plaque in the arteries of the heart.3
In fact, research shows that LDL cholesterol is not associated with higher rates of cardiovascular disease (CVD). One review article on the topic concluded, “the idea that high cholesterol levels in the blood are the main cause of CVD is impossible because people with low levels become just as atherosclerotic as people with high levels and their risk of suffering from CVD is the same or higher.”4 Further, and more pertinent to my situation, 75 percent of people admitted to the hospital having a heart attack have normal or optimal LDL levels,5 and a growing number of heart attack events are happening in people without high cholesterol.6
In my opinion, LDL-cholesterol and total cholesterol in the blood do not reflect risk for heart disease. Measuring cholesterol in the blood provides insight about only the current metabolism taking place. One group of researchers has described increases in blood lipid levels when relying more on fat for energy (that is, a lower carbohydrate diet)7 and decreased LDLcholesterol when including more glucose and other carbohydrates for a fuel source.8 Thus, the focus on lowering LDL to prevent heart disease is not likely to be effective. A study that reviewed twenty-one clinical trials on the efficacy of cholesterol-lowering medications for preventing heart disease and heart attacks found that cholesterol-lowering drugs have very little benefit and that their benefits are largely overstated due to misleading statistical presentation of the data in the studies.9
REFRAMING THE QUESTIONS
The conventional theory of what causes heart attacks is that cholesterol builds up in the arteries of the heart in the form of plaque and slowly blocks an artery. However, if total cholesterol and LDL-cholesterol are just a reflection of metabolism and are not the cause of heart disease, and if lowering them doesn’t prevent heart disease, what does cause plaque to develop in the arteries? We know that cholesterol is not the driver of plaque formation, but plaque does still occur.
There is plentiful research suggesting that atherosclerotic plaque in the walls of arteries is a result of a clotting response in the blood.10 One article states, “fibrin [clotting tissue] appears to be a multi-potential component of atherogenesis, intervening at virtually all stages of lesion development.”11 Fibrin is more or less the same clotting tissue response that forms in response to damage to your skin, such as a scab to stop bleeding. Researchers who analyzed the composition of plaque in arteries found that it was about 87 percent fibrotic clotting tissue.12 In a study of individuals with genetically high cholesterol, some of them developed plaque and some of them didn’t; the difference was that those who developed plaque had a genetic predisposition to elevated clotting factors in their blood.13
In 1856, Rudolf Virchow showed the world that what causes pathological clotting in blood is damage to the lining of a blood vessel, inadequate or altered blood flow and a situation where the blood becomes too thick or viscous.14 Medicine today still generally accepts these as the causes of clotting.
Medicine’s theory of heart disease says that if enough plaque builds up, it could lead to restricted blood flow and cause chest pain (angina) or block the artery enough to cause a heart attack. In addition, the thinking is that unstable, or soft plaque could rupture and cause an acute blockage. However, there is evidence that even with the presence of plaque, neither one of these situations is likely to cause a heart attack.
There are various tests used to measure the amount of plaque in the arteries of the heart and how narrowed the pathway for blood has become due to that plaque. One such test is a coronary artery calcium (CAC) scan, which measures the amount of calcified plaque in the arteries. Studies show that the higher the CAC score, the greater the risk of a heart attack.15 The conventional explanation is that this is because more plaque in the arteries increases the chances of someone getting to the point where an artery closes or the plaque ruptures and causes a heart attack. However, the work of Italian researcher Giorgio Baroldi (1925–2007) forces us to question these ideas.
THE BODY KNOWS WHAT TO DO
Dr. Baroldi, a cardiovascular pathologist, spent most of his career investigating the coronary arteries but, as far as I can tell, the field of cardiology has largely ignored his work. He developed a method to cast the arteries of the heart in autopsy with a plastic material so that when he dissolved away the heart tissue, he was left with a perfect representation of the arterial system of the heart, including very small arteries that do not show up on angiogram imaging.
When he studied the casts, what Baroldi found was astonishing. Any time the narrowing of an artery due to plaque got to about 70 percent, the body built collateral arteries around the narrowing that fully compensated the heart tissue with blood.16 In his book summarizing this work, Baroldi stated, “any severely obstructed coronary artery lesion, even multiple ones, was always found associated with enlarged collaterals.” 17 These collateral arteries can form very quickly, within four to seven days.18,19 Figure 2 illustrates the formation of these arteries; Figure 3 is an image of the collaterals in one of Baroldi’s plastic casts.
When doctors did a heart catheterization procedure on me in the emergency room, they found a 100 percent blockage in the LAD artery. If this blockage had developed slowly enough, according to Baroldi’s work, I should have developed collaterals. Because I was indeed having a heart attack, the blockage must have formed very quickly—perhaps even instantaneously—leaving no time for collateral arteries to form. Conventional medicine says that in a heart attack, a rupture of plaque occurs, which initiates a clotting response large enough to block the artery instantaneously. However, an article reviewing evidence on the plaque rupture theory of heart attacks found that while plaques do rupture, the ruptures cause heart attacks much less frequently than generally thought, with an estimated event rate associated with each plaque of “only 0.06 percent per year.”20 Discussing how plaques rupture, the article states that the clotting tissue formed to heal them contributes to further narrowing of the artery with plaque. But Baroldi’s work shows us that if this happens over time, the body will build collaterals to ensure that the heart tissue gets enough blood.
Baroldi’s findings on collaterals and the fact that plaque ruptures are rarely the cause of heart attacks help explain why the procedures that Western medicine uses to try to prevent future heart attacks—like placing preventive stents (to open up a narrowed artery) or conducting bypass surgeries (using a vein to direct blood around a narrowing)—are not achieving their stated aim.21,22 If the body is going to build collaterals and maintain blood flow, and if plaque ruptures rarely cause heart attacks, then opening up a narrowed artery with a stent or creating a new route with a bypass is not going to help. These procedures do seem to alleviate symptoms in some people, but in my opinion, they should never be done for the sake of trying to prevent heart attacks in those without symptoms. Some researchers have described the continued use of expensive and profitable procedures that do not prevent future heart attacks as “the elephant in the room” in cardiology.23
NO-BLOCKAGE HEART ATTACKS
In the paper showing that plaque ruptures rarely cause heart attacks, the authors contend that medicine should shift away from treating narrowing in the arteries and instead focus on preventing clotting in the arteries. I agree. In my lecture at Wise Traditions 2024, titled “The Biophysics of Heart Disease and Covid Injection Clotting,” I discussed the role of structured water and infrared light in protecting us from atherosclerosis through their prevention of clotting.
It is well known that one of the biggest risk factors for clotting in the bloodstream is stagnant or interrupted blood flow.24,25 When thinking about what caused my heart attack, it’s possible that plaque development in the LAD was interrupting blood flow. I was likely dehydrated at the time, as I was dealing with constipation. Dehydration has been shown to negatively affect blood flow by making the blood thicker or sludgy.26 Moreover, about thirty-six hours before the event, I had received stressful family news, and that situation was still unresolved at the time of the heart attack. Stress, too, has been shown to increase clotting risk.27 Combined with some plaque build-up already present, these factors could have created the perfect storm for a clot to form instantaneously without enough time for collateral formation.
Six months prior to my heart attack, a CAC scan had given me a perfect score of zero, meaning that there was no calcified plaque in the arteries of my heart. So, while an acute clot forming due to thicker blood trying to get around already existing plaque build-up could have been the mechanism behind the heart attack, with no calcified plaque present, there could have been another cause as well. Figure 4 again shows my angiogram image from the time of the heart attack, but this time, the arrow is pointing to an area just downstream from the blockage in the artery. It seems to be filled with blood. You can also see that the artery branches downstream from this area seem to have less than adequate blood flow. When a heart attack happens, heart tissue dies, generally thought to be from a lack of blood to that area of the heart. Based on this image, the branches of arteries downstream from where the arrow is pointing don’t have much blood in them, which means the heart tissue they supply isn’t getting enough blood. If this tissue is starving for blood, then why is blood upstream just sitting there? Why is that blood not going down into the heart tissue that is dying due to lack of blood? It’s almost as if the blockage and something happening in the heart tissue are keeping the blood trapped in the artery where the arrow is pointing. How can we explain this?
As it turns out, another type of heart attack, called “myocardial infarction with non-obstructed coronary arteries” (MINOCA), happens without any blockage. Although medicine seems to have no real understanding of the causal mechanism and generally considers this type less common,28 in my research, I have discovered potential mechanisms suggesting that MINOCA may be much more common than acknowledged.
THE ROLE OF STRESS
The cascade of events that leads to MINOCA is largely triggered by a dysfunctional stress response in the autonomic nervous system (ANS). Our evolved stress response is supposed to be activated only when it needs to be (such as when our life is in danger), but the mismatch between how our stress response evolved and our unnaturally stressful modern environment can cause the stress response to become imbalanced. Instead of healthily going back and forth between a stress response and a non-stress state, we can get stuck on constant high alert, altering ANS signaling.29 This could explain why heart attacks are more prevalent on stressful days of the year and on Mondays when people go back to work,30 as well as why heart attacks spike around the time of the daylight savings time change, which is stressful to our nervous system.31
The ANS consists of two parts: the “rest and digest” (parasympathetic) side, which is more active in non-stress situations, and the “fight or flight” (sympathetic) side, reserved for those times when a stress response is necessary. Normally, a surge in one includes a lesser surge of the other to maintain balance. The signal for this system is conducted through the vagus nerve. Although a combination of factors has to converge for a heart attack without a blockage to occur, an out-of-balance ANS is a key trigger.
The control of ANS balance in heart tissue relies on two messenger molecules: cAMP and cGMP. cAMP levels rise in the heart cells when we have a stress response, and cGMP levels rise when we are in a relaxation state. When it comes to cGMP (the relax molecule), there is one critical difference: nitric oxide or NO (produced in the cells of the walls of arteries called endothelia)32 is needed to increase its levels. When we experience a stress response and the nervous system causes spikes in cAMP within the heart, then—provided there is enough NO—cGMP also increases to keep the system in balance33 (see Figure 5).
Think of it like this. If you are walking your dog, and your dog starts to run after your neighbor, holding onto the leash is what prevents a bad outcome such as your dog attacking your neighbor. Your dog’s reaction is like the stress signal of cAMP, and you holding the dog back on the leash is the balancing response of cGMP. If this process works, then all goes well.
When we have prolonged periods with surges of stress responses that increase levels of cAMP, and there is not enough stimulation of the relax response, then we can lose the ability to move effectively between the two states and can get stuck in a stress state. This is called “decreased vagal tone” because the vagus nerve carries the non-stress signals.
Heart rate variability (HRV) is the best measure of balance in our stress response. The higher a person’s HRV, the more balanced they are. Interestingly, one study showed the complete suppression of HRV preceding 95 percent of ischemic heart attack events (see Figure 6).34,35
When our stress response becomes imbalanced, the fail-safe within the cardiac cells is supposed to be that consistently high levels of cAMP are balanced by also rising levels of cGMP. Again, however, cGMP can do this only if NO is present. If NO gets depleted because our body is in an inflammatory state or the lining of the artery is impaired,36 this can increase the chances of having a stress response without the balance of the non-stress response. In other words, the dog is able to go after the neighbor because you don’t have the dog on a leash.
THE BIG EVENT
When humans experience decreased vagal tone for long periods while also experiencing decreases in NO levels, this can cause a surge in the stress response and subsequent elevation in cAMP in our heart cells without a balanced rise in cGMP (see Figure 7).35 This can set into motion the cascade of events that is a heart attack without a blockage.
The sudden unchecked rise in adrenaline from the stress response causes an increase in lactic acid production within cardiac cells.37 This happens because the stress response situation persuades the heart, which usually prefers to burn fatty acids and ketones,37 that it needs to burn energy more quickly. It is quicker to burn glucose than to burn the more efficient and preferred energy source of fats and ketones.38 Burning glucose causes a build-up of lactic acid and hydrogen ions within the heart cells, creating a state of acidity. Studies show that the production of lactic acid is increased by a factor of eight in this situation, with no change in oxygen levels.35 This is similar to doing a sprint or a hard, fast workout; lactic acid builds up in the muscles, causing the muscles to have that burning feeling, but oxygen levels are not affected.
In the legs or arms, if we stop moving the muscles, the lactic acid will move along, discontinuing the build-up and the burning. However, the heart can’t just stop contracting, so the rapid build-up of lactic acid in the heart tissue causes a major problem, preventing calcium from being able to bind to muscle fibers to create contraction of the heart muscles.39 Low calcium in heart cells results in slower conduction velocity and elevated arrhythmia risk.40 This eventually leads to decreased muscle tension and contractility, which then causes a stretching of the wall of the heart that leads to increased pressure.41 The increased pressure in the tissue prevents blood supply from getting to the tissue.42 This results in very quick tissue death before any drop in oxygen is seen in heart tissue—in other words, a heart attack.
Once again considering my angiogram image (Figure 8), it’s plausible that these events could have taken place. The complete blockage (A in Figure 8) could have been there well before the heart attack, but collaterals (which are too small to visualize on angiogram imaging) could have formed around it, supplying blood to the area after the blockage (B in Figure 8) and preventing me from having any symptoms of poor blood flow. The stress I was under, which created two poor nights of sleep, imbalanced my nervous system response. In that state, when I did a high-intensity interval training workout on the morning of the heart attack, it could have been the proverbial straw that broke the camel’s back, creating a stress response that caused the swelling of the heart tissue supplied by the arteries (C in Figure 8). This prevented blood from entering the heart tissue and caused the blood to pool up at B.
Was this what caused my heart attack? I don’t know. When they placed a stent to open up the blockage, my heart attack symptoms immediately went away, which could make one think that the blockage was the cause. However, they also administered morphine, which would have made the pain better and could have calmed the nervous system response and allowed for rebalanced signaling to the heart tissue, stopping the process of heart tissue death.
I will likely never know which of these two situations caused my heart attack, and I don’t feel that I need to. F. Scott Fitzgerald once said, “the test of a first-rate intelligence is the ability to hold two opposed ideas in the mind at the same time and still retain the ability to function.” I do not have to know which situation caused my heart attack to put myself in the best environment to prevent it from happening again.
MAINTAINING HEART HEALTH
The strategies I use to create the best chance for heart health are helpful in preventing heart attacks in both scenarios—the acute clotting scenario and the imbalanced stress response scenario. To decrease risk of acute clotting, we should do things that help keep blood moving and keep it from getting too thick or viscous. To decrease risk of an imbalanced stress response, we should do things that improve HRV. There are strategies that do both of these things.
In my opinion, the strategies that have the most impact on the causes of heart attacks are not diet-related. Among all the things I recommend, the most important are to focus on sunlight and grounding. For life on Earth to sustain itself, it needs to harvest energy from its environment and use it to create the order that we call “health.” The source of all the energy for life on Earth is the sun. Thus, it makes sense that sunlight exposure would be good for us. The sun emits 40 to 50 percent infrared light any time that it is up, and infrared light is most effective at structuring water in the body. Structured water in blood vessels is a primary driver of blood flow.43 Getting sunlight has been shown to increase blood flow in the body.44 Further, getting sunlight exposure and setting your body to the day/night cycle of the sun (by being cognizant of artificial light exposure when the sun is not up) have been shown to improve HRV.45
Infrared saunas and red/infrared light panels are other ways to boost infrared light exposure if you are unable to get enough sunlight.
Red-light therapy and infrared sauna are both effective at increasing blood flow.46,47 Sauna use also increases HRV.48
Grounding is another way to gain energy from the sun. The sun continuously transfers electrons into the ionosphere (the upper atmosphere of Earth that holds ions). During times of excitement (storms), lightning discharges ions and keeps the earth full of negatively charged energy. Physics teaches us that when two conductive entities touch each other, if there is a difference in charge between the two, electrons will flow from the entity with the higher concentration of energy into the entity with the lower concentration.49 Living creatures are conductive surfaces, and the earth is a conductive surface. When we put bare skin on the ground, we soak up electrons through the hydrated fascia network in our body, and these are transported to be used in the mitochondria of any cells that need it.50
Direct contact with the earth is the best way to ground, but there are also devices that connect to the grounding wire of an indoor outlet. These are often used in research studies. A study that had subjects do six weeks of grounding found that HRV was much higher on average in the grounding group versus the control group.51 Another study investigated the effects of grounding on vagal tone (HRV) and survival in infants born preterm. Vagal tone increased 67 percent and improved the infants’ resilience to stress (and, therefore, their ability to survive).52 Lastly, a study tested the effect of grounding on HRV by grounding subjects for forty minutes, designing the study so that participants did not know who was being grounded and who was in the control group. The grounded group experienced an increase in HRV that continued to improve throughout the forty minutes of the experiment.53 These studies clearly illustrate how connecting to Earth’s electrical field can improve HRV and increase coherence.
Grounding increases blood flow,54 conducting energy not just local to the surface of the body but throughout the body.55 Grounding also increases the structured water found on the elements of blood, called zeta potential.56 Maintaining a strong electrostatic attraction between the fluids in the body and the elements in that fluid—by maintaining the zeta potential of the blood elements—increases blood flow and keeps blood from clumping together and clotting.
Sunlight and grounding are important because they are done outside. I think it is no accident that the rise of heart disease and heart attacks seen since the 1950s correlates with the invention of brighter indoor lighting, which has led to a life lived to an ever greater extent indoors. The average person today spends about 93 percent of his time either inside or in an enclosed vehicle.57 Our bodies are starving for the energy that we get from being in the sun with our feet on the earth.
Discussion about the prevention of heart disease and heart attacks tends to be dominated by the topic of diet. This is mostly due to the unfounded linking of heart disease with cholesterol and the fact that cholesterol is found in food. In my view, the only way that diet can contribute to heart disease is if someone is eating a processed-food diet full of toxins. The most important thing to do is to center the diet around naturally raised animal foods and whole plant foods in season.
Of course, many things will improve our health and prevent disease. In addition to eating whole foods in season, factors include staying hydrated, avoiding toxin exposure, resolving past traumas, exercising, expressing gratitude and avoiding non-native electromagnetic signals. I feel that the most important thing to do is spend more time outside. This is the way it was for humans before our modern way of life. After my heart attack, my diet and “high” LDL levels stayed the same and I continued to go through a personally stressful time for eighteen months. However, taking no medications other than a blood thinner for six months, my heart function and tissue completely recovered during the two years after my heart attack, and I reversed a 70 to 99 percent narrowing of plaque in an artery in my leg. Imaging showed that the arteries of my heart remained almost completely free of plaque. The only behaviors I changed and practiced consistently during this time of healing were getting sunlight, grounding, using my infrared sauna and being very conscious of artificial light exposure before sunrise and after sunset to sync my body up to the day-night cycle of the sun and stimulate healing. This is the power of reconnecting with nature.
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This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly journal of the Weston A. Price Foundation, Fall 2025
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