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Can You Die of a Broken Heart?

Updated: Sep 27, 2019

There is a true story out of ancient Arabia about a 7th century poet named Qais ibn Al-Mulawah. The story is famous in Arabic literature and is called Majnoon Lila, which means “crazy about Lila”. Qais had fallen in love with a girl named Lila, and she loved him back, but her father would not consent to the marriage. He forced Lila to marry someone else and Lila and her new husband moved away. The heartbroken Qais exiled himself to live in the desert. He lost interest in family, friends, and society and wrote poems describing his despair. He wrote of sleeplessness, fainting episodes, lack of appetite, and heart palpitations. The story goes that he died immediately after writing these words:


"My heart is firmly seized

By a bird's claws;

My heart is tightly squeezed,

When Lila's name flows.

My body is tightly bound,

My body is tightly bound,

Is like a finger ring around."


Arabic illustration of Majnoon Lila


Dr. H.A. Hajar Albinali, a modern-day cardiologist who translated that poem to English and authored the book, Majnoon Lila: Between Medicine and Literature, claimed that this was the first documented description of angina in the history of medicine. He concluded, based on that poem and other documented symptoms, that Qais had coronary artery disease and died from myocardial infarction. (r)


In modern medicine we have called heart issues from heartache Takotsubo cardiomyopathy, or Broken Heart Syndrome. It even has an official ICD 10 diagnosis code. In medicine it is thought that Broken Heart Syndrome is different than a heart attack, yet Dr. Albinali thinks Qais seems to have died of a myocardial infarction from coronary artery disease possibly complicated by a broken heart. But did Qais have coronary artery disease? Is coronary artery disease necessary to have a heart attack? Can someone really die of a heart attack from a broken heart alone?


Most people think that all heart attacks are caused by blockages of coronary arteries. This is because western medicine has been preaching the stenosis or clot theory of a heart attack since the 1950’s. If you follow this blog, you know that I disagree that this is the cause of the majority of heart attacks and have written a lot about why. I explain if fully later in this post, but the gist is that heart attacks are caused by a specific series of events that ultimately arise from not being fat adapted, having high oxidative stress, and having an imbalanced stress response. (r) The emotional stress component demands a lot of attention and may be the single greatest driving force. As you can guess this will be the focus of discussion in this post.


To fully understand how a broken heart can cause a heart attack, we have to take a step back and learn about how our stress response evolved. Then we must look at how our current environment effects the normal functioning of that evolved stress response. In my book, The Health Evolution: Why Understanding Evolution is the Key to Vibrant Health, I argue that our chronic disease epidemic is the result of a mismatch between our evolved physiology and our modern human environment. Our stress response is no exception.


To start we need to be familiar with the evolved stress response of the animals that came before us mammals evolved, reptiles. When I say stress response, I mean the behavior exhibited when reptiles find themselves in a threatening situation. The part of the body in animals that is taking cues from the animals’ environment and then relaying the information to the animals’ brain telling it if it is in a safe or threatening environment is called the Autonomic Nervous System. The nerve that communicates this information throughout the body is called the vagus nerve.


When reptiles have a stress response, they have one of three reactions. They flee the scene, fight off the threat, or freeze. The flee is obviously to run away and the fight is obviously fight for its life, but what does freeze mean exactly? In essence, this reaction would be to play dead. This response is really only used when the stress response required was too much for the reptile to handle. I am not exactly sure how this became evolutionarily advantageous, but it must have been advantageous because aspects of this play dead reaction are still present in reptiles. As we will see it may even still be present to some extent in us mammals. If it had not been evolutionarily advantageous then this characteristic would have been selected out by natural selection a long time ago.


So, what does “play dead” mean physiologically. Reptiles are cold-blooded, this means that they do not have to maintain the body heat that a mammal has because they are not as metabolically active. This is very important when it comes to the freeze stress response. Because reptiles do not need to maintain body heat and high metabolic activity, like mammals do, they can make their freeze, or play dead response, pretty darn convincing. By this I mean that they can literally shut down organs or organ systems without dying in order to convince another living thing that they are indeed dead. In most reptiles there is a single pathway in the vagus nerve and it is what gets overstimulated in this freeze response. That pathway is the dorsal motor nucleus of the vagus nerve.

As evolution moved forward to more highly evolved reptiles, like turtles and crocodiles, we start to see the vagus nerve split into two pathways, though not completely. Those two pathways are the original dorsal motor nucleus and a newly evolved nucleus ambiguous. When the first mammals evolved the split was complete and though these two pathways are still both in the vagus nerve, they can operate separately. This is discussed in more detail in the work of Dr. Stephen Porges and his Polyvagal Theory. (r)


When it comes to the stress response of a mammal, like us humans, this split is very important. As we said before, reptiles can have an overwhelming stress response, where organs shut down temporarily, without the consequence of death because of their slower metabolism. Mammals, however, are much more metabolically active. They have body heat to maintain and they move around much quicker and for longer periods of time than reptiles. Because the Autonomic Nervous System that controls this signaling is an automatic system, meaning it is not under conscious control of the animal, it has an automatic response based on the information received from the outside world. This could be what that mammal sees, hears, touches, smells, tastes, and, in the case of humans, feels emotionally.

Now, because of the necessity of higher metabolic activity, a mammal could not have a freeze stress response like reptiles, where organ systems shut down, without dire consequences, like dying. Therefore, the complete split of the vagus nerve into the dorsal motor nucleus and the nucleus ambiguous took place. The newly evolved nucleus ambiguous allowed mammals to have a stress response in order to fight or flee the situation and not go into a freeze response that would damage their high metabolism dependent oragans. This system works fairly well for mammals when they are in their natural environment. We know this from the study of mammals in the wild today.


Dr. Robert Sapolsky, a neuroendocrinologist at Stanford, has spent a lot of time studying the stress response of mammals on the African savannah. He has found that when a mammal is not faced with a threatening situation, they have low stress hormones in their system. If a threat does present itself, like a predator, then the stress response hormones are released, the signal is transmitted through the vagus nerve, and the appropriate fight or flee behavior happens. If the situation turns out well for the animal and it manages to fight off or flee the threat successfully, the signs of a physiologic stress response go away completely within minutes. This is the way a mammal is supposed to respond to a threat.


The brilliance of Dr. Sapolsky is that he took this information and compared it to the stress responses that he saw in humans living in our modern society. He found that humans, with our highly evolved brains, are the only species on Earth that can think their way into a stress response. For the mammals in the wild, when the threat was gone their physiology went back to normal, almost as if the threat never happened. Alternatively, in humans, our higher-level thinking and the bombardment of unnatural stresses in our modern environment, can result in our bodies stress response physiology being turned on all day long.


We could have something stressful happen to us and instead of turning off the stress response after it was over, like the mammals in the wild, we could think about it the rest of the day. We could also see something stressful happen to someone else or in a far-off place in the world and think ourselves into a stress response just by thinking that it could happen to us too. As Sapolsky says, “If you’re constantly but incorrectly being convinced you’re about to be thrown out of balance you’re being an anxious, neurotic, paranoid, or hostile primate who is psychologically stressed.” (r)


Most peoples’ lives are not actually being threatened on a day to day basis, but we live in a society with constant demands. Because of the way our society is set up, if we do not meet these demands then our life could become very difficult and that is stressful. Sapolsky has found that we have low grade physiologically life threaten responses to this constant bombardment of unrealistic demands. Humans are the only species with the level of thinking high enough to think our way into a stress response.


Our stress response is the same evolved stress response that allowed for the evolution of higher metabolic activity which in turn allowed mammals to evolve. This happened 225 million years ago when we see archeological evidence of the first mammals. That stress response has been there for 225 million years, and the unnatural demands of modern civilization have only been around for the last 10-12 thousand years (which means Qais also lived in this mismatched of civilization). Therefore, there has not been enough time for us humans to evolve a stress response adapted for this modern environment.


Now, let’s start to draw this whole line of thinking back to our original question. It is obvious in our society that we associate the heart with emotion. There is a reason we say things like “I love you with all my heart” or “You gave it all you heart”. That reason is that the heart is very well innervated by our vagus nerve, I could argue more so than any other organ. In medicine it is thought that the vagus nerve only innervates the heart at the right atrium where the heartbeat signal is conducted. But it has been shown that the vagus nerve is connected to all areas of the heart allowing our emotional state to affect the entire heart. (r,r) Some fibers of the vagus nerve even innervate some muscles of the face. Our faces are how we convey our emotional state and interpret the emotional state of others.

The demands of modern society and the higher-level thinking that separates us humans from other mammals, as well as the emotional and anatomical connection of our heart to our psychological state, is starting to make the story of Qais and the idea of dying from heartache not so far-fetched. Though our split vagus nerve helps prevent us humans from having a freeze response like we saw in reptiles, the dorsal motor nucleus is still there. I believe the characteristics of that freeze response are still with it. I also believe the mechanism of what happens when we humans are put in a situation that defaults us back to that freeze response of the dorsal motor nucleus has been worked out as well. If you keep up with my blog this next part will be familiar.


The control of the balance of the autonomic nervous system in cardiac cells, and many other cells, relies on two messenger molecules called cAMP and cGMP. (r) cAMP levels rise in the heart cells when we have a stress response and cGMP levels rise when we are in a relaxation state. The only difference is that when it comes to cGMP, the relax molecule, something else is also needed to increase its levels. That something else is nitric oxide, NO, (r) which is produced in the walls of arteries. These two molecules—cAMP and cGMP—keep each other in check within heart cells, they should always balance each other out. When we experience a stressful response and the nervous system causes spikes in cAMP within the heart then cGMP, provided there is enough NO, also has an increase just to keep the system more in balance. (r) This is depicted in the image below.



Sroka, K. (2013). What is the connection between oxidative stress and heart attacks? Retrieved from heartattacknew.com/faq/what-is-the-connection-between-oxidative-stress-and-heart-attacks/

But the system can become unbalanced. When we have prolonged periods in our life with many surges of stress responses (like a few weeks of broken heart) that increase levels of cAMP and not enough stimulation of the relax response and cGMP, then we can lose the ability to effectively balance these two states. We can get stuck in our stress state. This is called decreased vagal tone. When this happens the failsafe within the cardiac cells is that those consistently high levels of cAMP are balanced by also rising levels of cGMP. But remember that cGMP can only do this if NO is present. If NO gets depleted from oxidative stress, it is really bad news.


When humans experience decreased vagal tone for long periods of time while also experiencing decreases in NO levels, then during a stress response this can result in a surge in the stress response and subsequent elevation in cAMP in our heart cells without the balanced rise in cGMP. This is shown in the image below.


Sroka, K. (2013). What is the connection between oxidative stress and heart attacks? Retrieved from heartattacknew.com/faq/what-is-the-connection-between-oxidative-stress-and-heart-attacks/


When this happens the cascade of events that is a heart attack plays out. The sudden unchecked rise in adrenaline from the stress response has been shown to cause an increase in lactic acid production within cardiac cells. (r,r) This happens because the heart usually prefers to burn ketones—a product of burning fat—but in this situation the body thinks it needs to burn energy quicker to get away from a threat. Since it is quicker to burn glucose the heart cells revert to burning it rather than burning the more efficient and preferred energy source of ketones. (r,r,r) Burning glucose causes the build-up in lactic acid and hydrogen ions within the heart cells. This is similar to when you do a sprint or a hard, fast workout, lactic acid builds up in the muscles causing the muscle to have that burning feeling.


When this occurs in a muscle in the legs or arms we can just stop moving it and the lactic acid and hydrogen ions will move along stopping the build-up and burning feeling. Since the heart can’t just stop contracting the lactic acid quickly builds up causing a major problem. The presence of acid in the heart tissue causes swelling in the area of tissue forced to burn glucose. (r) This swelling creates a higher pressure in the tissue than there is pressure from the blood flow into heart tissue and therefore prevents the blood from reaching the cells. This explains why nearly 100% of heart attacks happen in the left ventricle. (r) The left ventricle is under the most pressure and is more susceptible to any changes in pressure caused by this edema. Without blood, this leads to dysfunctional cells walls and heart tissue death. In other words, a heart attack.


Could this situation be an overstimulation of the evolved nucleus ambiguous of mammals and the nervous system reverting back to the still present dorsal motor nucleus mechanism of stress response of reptiles? Could this be the mechanism by which reptiles have a freeze response only they experience no harm because of their slower metabolism? Could this be what happened to our dear heartbroken Qais?

Given the evolved stress response we have and the mismatch between that stress response and our modern world, it seems feasible. Add to that the fact that we humans have a complex and intense system of emotions that other mammals who share our same evolved stress response don’t have. Ask anyone who has ever experienced extreme grief or heartache and they will tell you it is the most intense emotion. People even often describe heartache as feeling like they have been stabbed through the heart. Modern science even shows us the connection between this and the heart.


The fact that western medicine recognizes a condition called Broken Heart Syndrome and that it is characterized by heart irregularities is proof of the effect of emotions on our hearts. Also, when we are heartbroken we tend to isolate ourselves, like Qais did to the extreme in the desert, and isolation has been associated with higher prevalence of heart attacks. (r) Lastly, studies have shown that Heart Rate Variability, the best measure of autonomic nervous system balance, drops significantly in the time leading up to a heart attack in 95% of people who have a heart attack. (r) Qais’ despair was so great that he thought his way into a chronic stress response and caused his body to revert to the older dorsal motor nucleus response of the vagus nerve that caused his heart attack and death.


To end on a high note there are things that can help you prevent a life-threatening situation during heartache. They are the three things that I believe will help prevent heart attacks even if there is no heartache. They are making sure you are fat adapted by intermittent fasting and carbohydrate restriction, avoiding NO depletion by decreasing oxidative stress by avoiding toxin exposure and restricting carbohydrates, and increasing your vagal tone by spending time in nature, having many close meaningful relationships, and practicing some form of mindfulness.


In my opinion, the best strategy to get us through heartache is reaching out to others for support. I believe Qais’ downfall was the way he isolated himself.


Stay healthy out there!


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