How the Heart Can Be Exhausted From Depression and Anxiety

Shin

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A 1967 publication titled “Mortality of Bereavement” discovered that bereaved relatives had a 7-fold increased risk of dying within the following year. Despite that the cause of death was undetermined, this is the first scientific evidence indicating that extreme sadness kills.

Coined in 1991, Takotsubo cardiomyopathy — or broken heart syndrome — mimics aspects of a heart attack such as shortness of breath, fainting, and chest pain. But, oddly, they have no blocked arteries. Instead, some parts of the heart stopped moving and other heart muscles try to compensate for this. This turns the heart into an irregular shape, like that of an octopus pot — hence, the name “Takotsubo” (‘Tako’ means octopus and ‘tsubo’ means pot in Japanese). This condition is reversible but can be fatal at times. Takotsubo cardiomyopathy is triggered by intense emotions or stressful life events such as the death of a loved one and losing (or even winning) a lot of money. This is why “heartbroken” from sadness is a legitimate phenomenon.

Research advances further confirm that sadness, or more accurately emotional stress, destroys the heart in many ways. The mind-heart connection extends to far more than just the broken heart syndrome. Convincing epidemiological evidence ascertains that emotional pains can lead to heart diseases, the major killer worldwide, and this linkage is underpinned by biology.

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The Heart on Depression and Anxiety

Diabetes, hypertension, and smoking cigarettes are confirmed predictors or risk factors of heart diseases. So is clinical or major depressive disorder (MDD) that increases the risk of heart diseases by 169% to as much as 343%, based on a meta-analysis that harmonized data from 11 independent studies. Even healthy people with depressive mood has a 49% increased risk of developing heart diseases, as shown by the same meta-analysis.

MDD is about twice or thrice as prevalent in those with heart diseases than in the general population. MDD also complicates the health outcomes of heart disease patients — prolonging hospitalization, increasing rates of rehospitalization, and accelerating disease progression. More concerningly, MDD increased the risk of death in individuals who had experienced a heart attack by as much as 4-fold (400%) within the following 18 months. As Milena Gebska, M.D., Ph.D., and a cardiologist at the University of Iowa acknowledge: “Depression itself is an independent risk factor for adverse cardiac events in patients without known heart disease.”

Depression and anxiety, or MDD and generalized anxiety disorder (GAD), often co-occur in clinical settings, as elegantly written by Erman Misirlisoy, Ph.D. in his publication in Elemental. “When people feel sad about their life and past experiences, they can also become anxious about where their life is headed. And when they feel anxious about the future, they can also become sad about how their life is currently playing out,” explains Misirlisoy.

In a longitudinal study — with a fancy title of “Scared to death? Generalized anxiety disorder and cardiovascular events in patients with stable coronary heart disease: The Heart and Soul Study” — individuals suffering from GAD had a 62% higher rate of contracting heart disease within 5.6 years. Likewise, individuals with heart disease or a history of heart attack are more likely to be anxious and meet the criteria for GAD. And anxious patients with heart disease are twice as likely to experience cardiac adverse events and succumb to it. Similar research trends have also been documented the same with other anxiety-related disorders, namely panic disorder and post-traumatic stress disorder (PTSD).

So, depression and anxiety are predictors of heart diseases and cardiac death. WHY?

The reasons are manifold ranging from lifestyle to biology. For one, depressed and anxious individuals neglect caring for themselves. Motivation to eat healthily, exercise, or adhere to medications and health checkups dissipates. They also turn to alcohol and smoking as coping mechanisms. As depression and anxiety are always persistent, such behaviors easily become habitual — rendering the heart fragile and vulnerable to failure.

Thoughts or the state of mind have power over human physiology. Disruptive thinking or experiences of catastrophic life events are emotional stressors that activate the bodily stress systems — the sympathetic nervous system and hypothalamic-pituitary-adrenal (HPA) — like any physical stressors would. These stress systems have regulatory mechanisms to shut them down and do not cause any complications if transiently activated. But prolonged and persistent activation — as evident in depressed and anxious individuals — initiates cascades of detrimental consequences in the body.

  1. Excessive sympathetic (“fight or flight”) activities lead to a lower rate of noradrenaline removal from the heart. This causes irregularities in heart rhythms, blood flow, and blood pressure. As sympathetic and parasympathetic (“rest and digest”) activities work in turns, too much of one suppresses the other. Thus, the central element of the parasympathetic system — the vagus nerve — becomes dampened. As the vagus nerve bridges the heart and diaphragm to the brain, a switched-off vagal activity disharmonizes both the heart rate variability and breathing rhythm.
  2. A hyperactive HPA axis makes the adrenal glands release adrenaline and cortisol uncontrollably, leading to cortisol resistance. This concept is similar to that of insulin resistance wherein cells are no longer responsive to insulin and the body produces extra insulin in response. Elevated circulating levels of cortisol have system-wide negative consequences, such as inducing glucose intolerance, hyperlipidemia (excessive LDL cholesterol), and accumulation of visceral fats. These push the body into a condition of pre-obesity (or obesity) and pre-diabetes (or diabetes), which compounds to heighten the risk of heart diseases.
  3. An engaged HPA axis also stimulates inflammatory reactions in the body. Immune cells become alert in response to stress, but they can’t differentiate between physical and emotional stress. They release inflammatory chemicals to fight physical stressors — such as damaged/unused cells or microbial infections — as they would for emotional stressors. Prolonged and uncurbed inflammation damages the heart endothelium and increases platelet formation. Platelets are immune cells responsible for blood clotting; unregulated blood clot thus hardens arteries.

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Healthcare Practices

Routine screening of patients with heart disease for any psychiatric disorders is now a current healthcare recommendation by the National Heart Foundation of Australia. Physicians are starting to implement antidepressants or anxiolytics and cognitive behavioral therapy (CBT) as part of treatment for heart disease patients with mental signs in need of extra psychiatry care.

Data to this day, however, remains limited and sometimes contradictory as psychiatric medications may interfere with the inner workings of the heart. While CBT poses no harm, it still too early to determine which antidepressants suit best for heart disease patients. Treating clinical depression and anxiety is challenging in and of itself; all the more is heart disease-depression-anxiety comorbidity. This is another case of why prevention is best. Ironically, the Indian photographer and visual artist, Manoj Jadhav, said it well:

“Health does not always come from medicine. Most of the time it comes from peace of mind, peace in the heart, peace of soul. It comes from laughter and love.”

This article was originally published here.

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