Forget cholesterol—stress is the main cause of heart disease, as new evidence is starting to demonstrate.
Ken Wilkinson had no fears about his routine heart checkup. The levels of fatty acid lipids in his blood were normal, and his cholesterol readings were textbook perfect. Not surprising, really, for a man who ate tofu instead of beef and who always went for the healthiest options. He even ran the 15 miles to the clinic.
But when he got there, the cardiologist urged him to have emergency surgery. His arteries were badly blocked, and he was in imminent danger of a life-threatening heart attack.
It didn’t make sense, at least not according to the prevailing theory that heart disease is caused by eating fatty foods. Although Ken’s diet was exemplary, his cardiologist didn’t know he was grieving the death of his young son—and it seems his grief was damaging his arteries and heart.
Ken’s experience isn’t unique. Parents’ risk of a sudden heart attack is three times higher than normal in the weeks after the death of their child, and the risk remains 20 percent greater for years afterward, according to researchers who evaluated the heart health of 126,000 parents who had lost a child.1
The death of a child is one of the most stressful things we can experience, but other stresses can also cause cardiovascular disease (CVD). People who are socially isolated are 1.5 times more likely to suffer from heart disease, while those who suffer stress at work have a 1.3-fold higher risk. Stress, anger and depression can all trigger CVD, heart attack and stroke, say researchers at University College London.2
It’s not a new idea. English physician William Heberden noted in the 1700s that “angina is increased by a disturbance of the mind,” while a newspaper correspondent wrote in the London Times in 1872 that the rise in heart disease deaths was the result of “great mental strain and hurried excitement.” Even this year, a headline in the New York Times suggested that “stress may be your heart’s worst enemy.”3
Most cardiologists don’t agree. Instead, they hold to the diet-heart hypothesis, which maintains that saturated fat in our diet raises our levels of low-density lipoprotein (LDL) cholesterol, commonly called the ‘bad’ cholesterol, which clogs our arteries (atherosclerosis), restricts the flow of blood to the heart and eventually causes a heart attack or stroke.
The theory launched the multi-billion-dollar cholesterol-lowering statins industry and the rise of low-fat foods and drinks, but with scant supportive evidence. As one review put it: “Dietary recommendations were introduced for 220 million US and 56 million UK citizens by 1983 in the absence of supporting evidence from randomized controlled trials.”4
To come to this conclusion, researchers from RCSI University of Medicine and Health Sciences in Dublin analyzed 21 studies to discover the impact that statins had on reducing the risk of heart attack, stroke and death. In other words, when your levels of LDL cholesterol fall, does your risk of developing heart disease also diminish?
Many of the studies they reviewed had used relative risk as the measure of the drugs’ effectiveness, with several showing they reduced the risk of heart attack by 29 percent—but relative risk is a statistical sleight of hand routinely used by drug researchers.
If, for example, there’s an absolute risk that two people out of every hundred will develop heart disease, a drug that reduces the risk by 50 percent means that just one person in a hundred will have the problem. “Fifty percent” is a headline figure, but, in fact, the drug is helping just 1 percent of people.
When the Irish researchers applied the absolute risk measure across the studies, the benefits disappeared. From the drug helping 29 percent of people, its absolute risk benefit was just 1.3 percent.5
These results have a deeper significance and suggest that LDL cholesterol isn’t a cause of heart disease; although statins were lowering levels, they weren’t having any impact on the rates of heart attacks.
If a low-fat diet isn’t going to reduce your risk of heart disease, what should you be doing?
From The Clot Thickens by Dr Malcolm Kendrick (Columbus Publishing, 2021)
Despite the lack of solid evidence, the diet-cholesterol theory just won’t go away—but, then, neither does the idea that stress causes CVD. But, first, what do we mean by stress? Essentially, stress is any situation in which we feel we are no longer in control, or we feel overwhelmed. It can be caused by problems at work, in a marriage, financial problems, by the death of a child or loved one, and even by trauma that happened when you were a child, as Andrew Steptoe at University College London has suggested.2
Even the sudden stress from natural disasters can increase the rate of heart attacks. In 1994, the rate leaped five-fold on the day there was a major earthquake in California, while the rate of heart disease doubled in Athens immediately following the 1981 earthquake.
Office staff faced with a “high-pressure deadline at work” were six times more likely to suffer a heart attack in the first 24 hours after the deadline had passed.6
Major studies have confirmed these findings. The INTERHEART study, which monitors around 25,000 people, has found that stress at work increases the risk of a heart attack, and those most at risk faced continual stress.7
The PURE study, which tracked the health of more than 115,000 people, concluded that those who suffered high levels of stress over most of the 10 years of the trial were 22 percent more likely to develop CVD.8
Many attention-grabbing headlines use relative risk calculations to make an effect seem larger than it really is. For example, if the risk of a heart attack is two percent, and a new drug lowers that risk to one percent, this means the drug is actually preventing a heart attack in one in 100 people. However, the relative risk reduction is a massive 50 percent—and this is the number you’ll see used by drug companies.
Dying from a broken heart may be the stuff of romantic fiction, but cardiologists have found it actually happens. People who have suffered intense psychological distress—such as a death, a violent attack or major financial loss—show sudden damage to the heart that mimics an actual heart attack, usually one to five days after the event.9
A broken heart even has a medical name—takotsubo cardiomyopathy—and is a sudden weakening of the heart muscle, invariably triggered by acute stress, including physical exertion.
Brazilian cardiologist Quintiliano H de Mesquita took things a stage further with his myogenic theory. After treating thousands of patients who had suffered a sudden heart attack—yet whose arteries were clear—Mesquita concluded that a heart attack originates in the heart, and not from blocked arteries.
He had also noticed that anticoagulants, which clear plaque from blocked arteries, weren’t reversing unstable angina pectoris—severe chest pain—which is usually the stage before a heart attack. Instead, cardiotonic drugs—such as digoxin and digitoxin—had been used for years to successfully treat angina pectoris and heart attack by making the heart itself more efficient and improving its ability to pump blood.
According to Mesquita, the hardening of the arteries (atherosclerosis), central to the dietary cholesterol theory, happens when the heart starts to fail and cannot push enough blood through the arteries to keep them pliant.
Instead, artery health has little to do with heart disease. Part of the heart can be weakened by all the usual suspects, such as smoking, high blood pressure (hypertension) and diabetes, because they trigger the release of stress hormones, such as adrenaline. Sudden stress can be the final blow to a part of the heart that has already been weakened.
Heart disease is still a mystery. Even though statin drugs recently reached $1 trillion in sales worldwide and low-fat foods aren’t far behind, CVD is still our major killer. Evidence that saturated fats don’t raise levels of LDL cholesterol continues to mount, although processed foods may have a part to play.
Stress in its many forms looks more like the key culprit, as we’ve intuitively felt all along, but even then, stress is subjective. What one person can handle with ease will make another a quivering wreck.
Despite these reservations, more die from a broken heart than from cholesterol.
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References |
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1 |
PLoS Med, 2021; 18(9): e1003790; Annu Rev Public Health, 2013; 34: 337–54 |
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2 |
New York Times, Jan 3, 2022 |
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3 |
Open Heart, 2015; 2(1): e000196 JAMA Intern Med, 2022; doi: 10.1001/jamainternmed.2022.0134 |
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4 |
J Epidemiol Community Health, 2005; 59: 23–30 |
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5 |
Lancet, 2004; 364(9438): 953–62 |
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6 |
JAMA Netw Open, 2021; 4(12): e2138920 |
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7 |
J Am Coll Cardiol, 2018; 72(16): 1955–71 |
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