Stress and Your Heart: The Mind-Body-Micronutrients Connection – Part 1

There is a common perception that stress has many negative health effects, including an increased risk of heart disease. This has been supported by data from epidemiological and clinical studies, as well as animal models, that show a connection between emotional stress and the likelihood of developing cardiovascular disease, accelerating its progression, and triggering adverse outcomes.

How our body responds to stress

Stress is a normal and expected part of daily life. Our body can handle challenging situations by unleashing the so-called “fight-or-flight” response, in which it shifts its functions toward survival mechanisms in the moment while slowing down other processes, such as digestion. When facing stress, our nervous system sends signals to the adrenal glands to release stress hormones such as cortisol, adrenaline, and norepinephrine, which speed up breathing and increase heart rate and blood pressure. We all know that the impact of stress is individual, and not all types of stressors – ranging from traffic jams, financial problems, or job interviews to dramatic life situations – are perceived similarly by everyone. The balance between cortisol, norepinephrine, and adrenaline is critical for one to feel well, especially under stress.

However, stress experienced for weeks at a time or longer starts to have a negative impact on the body. Hormonal changes associated with chronic stress will, over time, exhaust the adrenal glands and affect the heart and blood vessel system by causing (or worsening) heart disease, increasing blood pressure, sugar, or cholesterol levels, provoking heart palpitations, and increasing inflammation. Long-term stress can speed up plaque development in the heart arteries (atherosclerosis) and trigger angina, stroke, or a heart attack. A study evaluating over 3,000 adults of mean age 40.2 years, with no prior cardiovascular events, concluded that chronic stress related to work, finances, relationships, or health issues, lasting more than six months, resulted in adverse cardiovascular events in 220 people and a lower chance of survival (1).

Stress can induce cardiovascular problems by impacting the body in different ways:

Dietary patterns: Stress can influence our appetite, how much we eat, and the types of food we are likely to choose. Often, chronic stress prompts overeating and the consumption of highly processed foods rich in fat and sugar. The interactions between stress and eating patterns can enhance neuroinflammatory responses, affect memory, alter gut microbiota, and ultimately create a predisposition to the development of obesity, cardiovascular problems, diabetes, and metabolic syndrome. However, for some people, chronic stress leads to reduced appetite and can contribute to depression.

Consequences of long-term inflammation: The fact that cardiovascular events and stress-related emotional disorders share a common epidemiology may indicate the existence of biological pathways linking these two diseases (2). Interestingly, some theories imply that our genetically developed response to adversity is effective in managing acute stress but not chronic social stress. Under long-lasting stress, the body’s response becomes inadequate and leads to chronic inflammation and disturbed metabolic functions (3).

Indeed, blood markers of inflammation, as well as decreased serum levels of anti-inflammatory omega-3-type polyunsaturated fatty acids, have been found in both depression and heart disease. Inflammation accompanying both cardiovascular disease and depressive disorders negatively affects lipid profiles, such as low HDL cholesterol (“good cholesterol”). Additionally, oxidative stress and accelerated cellular aging implicated in anxiety and depression can exacerbate cardiac problems (4).

In addition to long-lasting stress, repeated exposure to short-term stress may cause permanent injury to the lining of blood vessels and trigger atherosclerosis. The largest and most comprehensive study investigating the effects of mental stress in patients with heart disease found that the induction of mental stress was associated with blood vessel constriction (high blood pressure), a prolonged increase in arterial stiffness, and endothelial dysfunction (5). Similar findings were also reported in smaller studies of individuals who did not have prior heart problems.

Impaired immune response: Stress-activated release of stress hormones and neurotransmitters modulates the function and movement of immune cells. While acute stress can temporarily strengthen immunity and promote protection during infection, chronic stress disturbs or inhibits immune function.

The inflammation connection

It appears that the biological connection between psychological stress, immunity, and cardiovascular disease is mediated through oxidative stress and inflammation, which harm DNA, increase lipid peroxidation, and damage the endothelial lining of blood vessels. This can trigger the development of vascular plaques, the cause of heart attacks.

The heart is not immune to infections. Viruses such as influenza, SARS-CoV-2 (the cause of COVID-19), or West Nile virus can cause inflammation of the heart muscle (myocarditis). This condition can damage the muscle and nerves in the heart, making it more difficult to pump blood, and can cause chest pain or irregular heartbeats. Heart inflammation can also lead to cardiomyopathy, manifested by thickening of the walls of the heart, which can result in heart failure.

Chronic stress-related systemic inflammation, in which the body is essentially attacking itself, not only causes illness but also inhibits our ability to recover from disease. Stress is directly correlated with worse wound-healing outcomes, with studies showing that it causes the healing process to take longer than it otherwise would. Some data have even indicated that 75-90 percent of human diseases are related to activation of the stress system.

Other aspects

There are many aspects that deserve further attention, such as how autoimmune disorders or vaccine efficacy are affected by long-term stress, as well as gender- and age-related stress responses. It has been observed that in women with stable cardiovascular disease, a stress-induced increase in the pro-inflammatory IL-6 level was significantly correlated with adverse cardiovascular events, while there was no such association among men. A similar female-specific relationship was found for another pro-inflammatory factor, chemokine monocyte chemoattractant protein-1 (MCP-1), which attracts or enhances the expression of other inflammatory factors and cells. An increase in MCP-1 (also known as CCL2) has been related to various diseases, including novel coronavirus infections, cancers, neuroinflammatory diseases, rheumatoid arthritis, and cardiovascular diseases.

REFERENCES

1. Ajibewa, Tiwaloluwa A., et al. Chronic Stress and Cardiovascular Events: Findings from the CARDIA Study. American Journal of Preventive Medicine, 2023; 67: 24-31.
2. Chauvet-Gelinier JC, Bonin B. Stress, anxiety and depression in heart disease patients: A major challenge for cardiac rehabilitation. Ann Phys Rehabil Med. 2017; 60(1): 6-12.
3. Epel E, et al. Accelerated telomere shortening in response to life stress. Proc Natl Acad Sci U S A. 2004; 101: 17312-17315.
4. Xue YT, et al. Investigating the role of acute mental stress on endothelial dysfunction: A systematic review and meta-analysis. Clin Res Cardiol. 2015; 104(4): 310-319.
5. Ghiadoni L, et al. Mental stress induces transient endothelial dysfunction in humans. Circulation. 2000; 102: 2473-2478.