The Heart-Damaging Effects of Stress

Controlling Cortisol for a Healthier Cardiovascular System
By VRP Staff

There is an enormous amount of medical literature on the deleterious effects of negative emotions (distress, depression, fear, anxiety, anger, hostility, etc.) on cardiovascular disease. Stressors can be acute (such 9/11 or Hurricane Katrina) or chronic (job stress, marital or relationship tensions, or the burden of care giving). Adverse cardiovascular effects in response to stressful situations can be severe, even fatal, and include the following:1-5

  • Increased heart rate
  • Elevated blood pressure
  • Increased oxygen demand on the body
  • Electrical instability in the heart, which leads to disturbances of cardiac rhythm (ventricular tachycardia, ventricular fibrillation, atrial fibrillation).
  • Spasms of coronary blood vessels, leading to myocardial ischemia (inadequate blood flow to the heart)
  • Myocardial infarction (heart attack)
  • Development of coronary atherosclerosis
  • Decreased heart rate variability (a measure of the beat-to-beat variations in heart rate).

In this article, we will focus on the way in which stress affects the heart and the neuroendocrine response to stress.

Stress and Cortisol—a Dangerous Combination

Psychological stress produces changes in the sympathetic-parasympathetic balance of the nervous system and alterations of the hypothalamic-pituitary-adrenal (HPA) axis, which negatively affects the cardiovascular system.3, 5-7

The HPA axis is a network of glands linking the brain and endocrine system that mediate stress and avert danger (producing the so-called “fight-or-flight” response). When a stressor is perceived, the hypothalamus, deep within the brain, secretes CRH (corticotropin-releasing hormone), which in turn acts on the pituitary gland to secrete ACTH (adrenocorticotropic hormone), triggering the release of cortisol from the adrenal glands. Under normal conditions, cortisol is involved in blood pressure regulation and cardiovascular and immunologic function; in response to stress, higher levels are secreted in order to facilitate energy production for optimal brain function. Increased cortisol production has been documented in several experiments measuring physiological responses to various stressors such as public speaking and mental arithmetic,8 noise and shock,9 and stressful events.7

The HPA axis is designed with a feedback control feature, so that when the danger or stressor has been averted, the hypothalamus halts the secretion of CRH, which ultimately restores cortisol levels to normal. However, during periods of prolonged stress, the “fight-or-flight” response of the sympathetic nervous system can go awry and remain constantly activated, resulting in chronic cortisol over-secretion and suppression of the calming parasympathetic nervous system.

It has been demonstrated that situations involving negative emotions result in impairment in feedback control of the HPA axis, leading to the release of chronically high levels of cortisol.7, 10 Elevated cortisol is a mediating factor in the development of heart disease and other medical disorders.2-5, 7, 10

Research over the past 50 years has shown that certain personality types such as 1) “Type A” (a combination of aggression, competitiveness, impatience, hostility, and anger);7 2) the recently proposed “Type D” or “distressed” personality (characterized by depressed mood, anxiety, anger, hostility coupled with social inhibition);7, 11-13 and 3) major depressives6-7, 11 are associated with a greater cortisol reactivity to stress, and therefore, higher rates of heart disease.

Emotions are so strongly linked to heart health that scientists estimate between 20 and 40 percent of sudden cardiac deaths are precipitated by acute emotional stressors.3

The Heart Disease Link

Cortisol is involved in many pathways that promote heart disease. For one, it inhibits growth hormone production, which is associated with a higher risk for premature cardiovascular disease.7 Second, by inhibiting the growth hormone and gonadal axes, it stimulates visceral fat accumulation,7 a precursor to metabolic syndrome, a potentially deadly combination of abdominal obesity, hypertension, low high-density lipoprotein, high blood sugar and insulin resistance. Metabolic syndrome is a potent risk factor for heart disease.14

In addition, the behavioral aspect of negative emotional states should not be underestimated. Unhealthy, stress-induced habits such as smoking, physical inactivity, poor diet and overeating can lead to overweight and metabolic syndrome, and ultimately, heart disease.

The Whitehall II Study

There are thousands of studies linking stress and heart disease, but one that stands out is the Whitehall II study, a large-scale prospective cohort study of over 10,000 English civil servants, aged 35 to 55, conducted between 1985 and 1988 in order to investigate the relationships between work, stress, and health. Dozens of investigators have examined the data, and multiple follow-ups have been performed, some still ongoing.

In this study published in the European Heart Journal, researchers reported a definite association between chronic work-related stress and coronary heart disease in the Whitehall cohort. They also reported that stressed workers were prone to physical inactivity, poor diet, the metabolic syndrome and its components, lower heart rate variability, and higher cortisol levels.

The study concludes, “Work stress may be an important determinant of coronary heart disease (CHD) among working-age populations, which is mediated through indirect effects on health behaviors and direct effects on neuroendocrine stress pathways.”15

This conclusion underscores the fact that stress affects the heart both directly, through HPA axis activation, as well as indirectly, through the development of unhealthy behaviors that precipitate dangerous conditions (overweight and metabolic syndrome), which in turn are risk factors for CHD.

In a related report of the Whitehall II study data, other researchers established an association between psychological distress, depression and an increased incidence of CHD.6

Preventing and Managing Stress

Negative emotions, as the above research shows, can set the stage for heart disease. There are a number of ways to take action to counter stress and lower cortisol by making some important behavioral and lifestyle changes:

  • Get regular exercise.
  • Eat a healthy diet rich in fruit, vegetables and whole grains
  • Don’t smoke
  • Drink alcohol in moderation
  • Practice stress management techniques such as meditation, yoga, biofeedback, progressive muscle relaxation, guided imagery
  • Seek social or professional support

In addition, targeted nutritional supplements have been shown to alleviate stress and anxiety. These include:

Withania somnifera, also known as Ashwaganda, is an adaptogen reported to have mood stabilizing,16 anxiolytic (anxiety-reducing) and antidepressant actions.16-17 It also has been shown to attenuate physiological stress responses18 and positively influence the endocrine and central nervous systems.19 Most recently, Withania was found to directly provide cardioprotective effects.20

Gamma-Aminobutyric Acid (GABA) is the major inhibitory neurotransmitter in the brain (i.e., it regulates brain excitability and nerve transmission). Either low GABA levels or decreased GABA function is associated with anxiety, depression, insomnia, and epilepsy.21 In human studies, GABA supplementation has been shown to induce relaxation and reduce anxiety.21-22

L-Theanine is an amino acid found in green tea that has long been used as a relaxant. In addition to reducing stress-induced physiological responses (changes in heart rate, sympathetic nervous system activation),23 this calming agent also decreases the brain’s production of excitatory neurotransmitters while increasing inhibitory neurotransmitters such as GABA.24

Valeriana officinalis, one of 250 species of valerian, has been used as a sleep aid and anti-anxiety agent since antiquity. Its antidepressant properties have also been described.25 It exerts a regulatory effect on the autonomic nervous system.26 and has been demonstrated to bind to benzodiazepine26 and GABA receptors,26-27 providing a tranquilizing effect, improving sleep quality and decreasing the time it takes to fall asleep.

Relora® is a proprietary blend of extracts of Magnolia officinalis and Phellodendron amurense. The active constituent of Magnolia officinalis, honokiol, exerts an anti-anxiety effect similar to that of the benzodiazepine, diazepam, without side effects.28 Recently, A U.S. Patent was granted for use of an extract of Magnolia officinalis for stress-related conditions involving elevated cortisol levels.

Berberine, the active component of Phellodendron amurense, demonstrates anxiolytic and antidepressant qualities.28 In a recently published study, Relora® was effective in reducing temporary, transitory anxiety.28 An earlier pilot study reported a reduction in cortisol levels and perceived stress.29

Using combinations of these stress-relievers, found in Allay™ (containing Withania somnifera, GABA, L-theanine, and valerian extract) and Cortisol Control (a synergistic blend of Relora® and Sensoril®, a patented extract of Withania somnifera), can help stabilize cortisol levels and increase relaxation. These effects can provide a strong foundation for a healthy heart.

Conclusion

The connection between negative emotional states and heart disease has been clearly established. Psychological stress, through activation of the neuroendocrine system, can have severe, even devastating effects. The good news is stress-related symptoms can be ameliorated and our health positively influenced through life-style changes, behavioral techniques, and the use of clinically proven natural supplements.

References

1. Ziegelstein RC. Acute emotional stress and cardiac arrhythmias. JAMA. 2007 Jul 18;298(3):324-9.

2. Dimsdale JE. Psychological stress and cardiovascular disease. J Am Coll Cardiol. 2008 Apr 1;51(13):1237-46.

3. Vlastelica M. Emotional stress as a trigger in sudden cardiac death. Psychiatr Danub. 2008 Sep;20(3):411-4.

4. Steptoe A, Brydon L. Emotional triggering of cardiac events. Neurosci Biobehav Rev. 2008 May 3.

5. Brotman DJ, Golden SH, Wittstein IS. The cardiovascular toll of stress. Lancet. 2007 Sep 22;370(9592):1089-100.

6. Stansfeld SA, Fuhrer R, Shipley MJ, Marmot MG. Psychological distress as a risk factor for coronary heart disease in the Whitehall II Study. Int J Epidemiol. 2002 Feb;31(1):248-55.

7. Sher L. Type D personality: the heart, stress, and cortisol. Q J Med. 2005 May;98(5):323-9.

8. Al’Absi M, Bongard S, Buchanan T, Pincomb GA, Licinio J, Lovallo WR. Cardiovascular and neuroendocrine adjustment to public speaking and mental arithmetic stressors. Psychophysiology. 1997 May;34(3):266-75.

9. Lovallo WR, Pincomb GA, Brackett DJ, Wilson MF. Heart rate reactivity as a predictor of neuroendocrine responses to aversive and appetitive challenges. Psychosom Med. 1990 Jan-Feb;52(1):17-26.

10. Todaro JF, Shen BJ, Niaura R, Spiro A 3rd, Ward KD. Effect of negative emotions on frequency of coronary heart disease (The Normative Aging Study). Am J Cardiol. 2003 Oct 15;92(8):901-6.

11. Steptoe, A, Molloy, GJ. Personality and Heart Disease. Heart. 2007; 93:783-784.

12. Denollet J, Pedersen SS, Vrints CJ, Conraads VM. Usefulness of type D personality in predicting five-year cardiac events above and beyond concurrent symptoms of stress in patients with coronary heart disease. Am J Cardiol. 2006 Apr 1;97(7):970-3.

13. Molloy GJ, Perkins-Porras L, Strike PC, Steptoe A. Type-D personality and cortisol in survivors of acute coronary syndrome. Psychosom Med. 2008 Oct;70(8):863-8.

14. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA. 2002 Jan 16;287(3):356-9.

15. Chandola T, Britton A, Brunner E, et al. Work stress and coronary heart disease: what are the mechanisms? Eur Heart J. 2008 Mar;29(5):640-8.

16. Bhattacharya SK, Bhattacharya A, Sairam K, Ghosal S. Anxiolytic-antidepressant activity of Withania somnifera glycowithanolides: an experimental study. Phytomedicine. 2000 Dec;7(6):463-9.

17. Gupta GL, Rana AC. Protective effect of Withania somnifera dunal root extract against protracted social isolation induced behavior in rats. Indian J Physiol Pharmacol. 2007 Oct-Dec;51(4):345-53.

18. Bhattacharya SK, Muruganandam AV.Adaptogenic activity of Withania somnifera: an experimental study using a rat model of chronic stress. Pharmacol Biochem Behav. 2003 Jun;75(3):547-55.

19. Mishra LC, Singh BB, Dagenais S. Scientific basis for the therapeutic use of Withania somnifera (ashwagandha): a review. Altern Med Rev. 2000 Aug;5(4):334-46.

20. Mohanty IR, Arya DS, Gupta SK. Withania somnifera provides cardioprotection and attenuates ischemia-reperfusion induced apoptosis. Clin Nutr. 2008 Aug;27(4):635-42.

21. No authors listed. Gamma-aminobutyric acid (GABA), Monograph. Altern Med Rev. 2007 Sep;12(3):274-9.

22. Abdou AM, Higashiguchi S, Horie K, Kim M, Hatta H, Yokogoshi H. Relaxation and immunity enhancement effects of gamma-aminobutyric acid (GABA) administration in humans. Biofactors. 2006;26(3):201-8.

23. Kimura K, Ozeki M, Juneja LR, Ohira H. L-Theanine reduces psychological and physiological stress responses. Biol Psychol. 2007 Jan;74(1):39-45.

24. Yamada T, Terashima T, Okubo T, Juneja LR, Yokogoshi H. Effects of theanine, r-glutamylethylamide, on neurotransmitter release and its relationship with glutamic acid neurotransmission. Nutr Neurosci. 2005 Aug;8(4):219-26.

25. Hattesohl M, Feistel B, Sievers H, Lehnfeld R, Hegger M, Winterhoff. Extracts of Valeriana officinalis L. s.l. show anxiolytic and antidepressant effects but neither sedative nor myorelaxant properties. Phytomedicine. 2008 Jan;15(1-2):2-15.

26. No authors listed. Valeriana officinalis, Monograph. Altern Med Rev. 2004 Dec;9(4):438-41.

27. Benke D, Barberis A, Kopp S, et al. GABA(A) receptors as in vivo substrate for the anxiolytic action of valerenic acid, a major constituent of valerian root extracts. Neuropharmacology. 2008 Jun 17. Published Online Ahead of Print.

28. Kalman DS, Feldman S, Feldman R, Schwartz HI, Krieger DR, Garrison R. Effect of a proprietary Magnolia and Phellodendron extract on stress levels in healthy women: a pilot, double-blind, placebo-controlled clinical trial. Nutr J. 2008 Apr 21;7:11.

29. Garrison R, Chambliss WG. Effect of a proprietary Magnolia and Phellodendron extract on weight management: a pilot, double-blind, placebo-controlled clinical trial. Altern Ther Health Med. 2006 Jan-Feb;12(1):50-4.

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