Health Hazards of Psychological Stress

by Ben Best

(For general perspectives, see Some Philosophizing About Psychological Stress.)




Psychological stress includes such things as worry, hate, anger, etc. Irritating noises, frustration in failing to accomplish tasks that are viewed with urgency, arguments with people, and having to deal with other people who are themselves stressed can cause psychological stress. Chronic grief can be stressful, often leading to depression. A rat model of depression is learned helplessness wherein a rat randomly receives electric shocks or is subjected to immobilizations that are beyond its control.

The physiologicical responses to psychological stress have much in common with physiological responses to physical traumas. The most notable hormonal responses are release of epinephrine (adrenalin) and glucocorticoid (cortisol in humans) with resultant elevation of blood pressure, blood glucose, etc. Like physical stress, psychological stress can be temporary (acute) or continuing (chronic). A small double-blind randomized 3-month study of substance abusers found that supplementing with omega-3 polyunsaturated fatty acids reduced anxiety and anger, with increased EPA more effectively reducing anxiety, and DHA more effectively reducing anger [PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY; Buydevis-Branchey,L; 32(2):568-575 (2008)].

Unlike physical stress, the sources of psychological stress are subjective. A soldier on a battlefield has much to worry about, but some will worry more than others (related to their personal risk-aversion) — and the same applies to civilians coping with daily life in peacetime. Persons with more imagination can have more worries on their minds, but not necessarily more anxiety.

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Obesity is both a cause and an effect of physiological and psychological stress. Most people eat more under psychological stress — and overweight people are especially likely to do so [TRENDS IN ENDOCRINOLOGY AND METABOLISM; Dallman,MF; 21(3):159-165 (2010)]. Insulin secretion is stimulated primarily by dietary sugar (glucose, not fructose) and complex carbohydrates, and secondarily by protein or fat. When both blood insulin and cortisol are high, fat and sugar become increasingly appealing, and ingestion of these foods can relieve the discomfort of psychological stress (which is why nibbling by persons experiencing the stress of dieting can lead to binge eating of "junk food"). Stressful "daily hassels" reportedly increase consumption of snacks high in fat and sugar [HEALTH PSYCHOLOGY; O'Conner,DB; 27(1 Suppl):S20-S31 (2008)]. High cortisol evidently increases appetite for sugar [PSYCHONEUROENDOCRINOLOGY; Epel,E; 26(1):37-49 (2001)] and fat [ENDOCRINOLOGY; la Fleur,SE; 145(5):2174-2185 (2004)]. Habitual stress-induced eating patterns can become a reflex that bypasses conscious decision-making.

Dietary fat and sugar primarily promotes visceral fat [TRENDS IN ENDOCRINOLOGY AND METABOLISM; Dallman,MF; 21(3):159-165 (2010)]. Visceral fat produces inflammatory cytokines that cause insulin resistance, which elevates blood fatty acids and promotes more insulin resistance (a viscious cycle, see Insulin Resistance and the Metabolic Syndrome and Molecular Mechanisms for more details). Elevated epinephrine in the bloodstream (which can be due to psychological stress) elevates blood glucose [JOURNAL OF CLINICAL INVESTIGATION; Stumvoli,M; 96(5):2528-2533 (1995)] which can increase insulin resistance (another viscious cycle). Stress increases insulin resistance more in people with more visceral fat (yet another viscious cycle) [AMERICAN JOURNAL OF PHYSIOLOGY; Darmon,P; 291(5):E995-E1002 (2006)]. Visceral fat is more sensitive to glucocorticoids because visceral fat has more glucocorticoid receptors. Subordinate monkeys have greater psychological stress, higher cortisol, and more visceral fat than dominant monkeys [AMERICAN JOURNAL OF PRIMATOLOGY; Shively,CA; 71(9):742-751 (2009)].

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High levels of stress-induced catecholeamines directly damage heart muscle ("broken heart syndrome"), and increase the risk of sudden cardiac death [FORENSIC SCIENCE INTERNATIONAL; Fineschi,V; 194(1-3):1-8 (2010)]. Glucocorticoids increase plasma levels of catecholamines, and increase sensitivity to catecholamines, thereby increasing cardiac damage [CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY; Adameova,A; 87(7):493-514 (2009)].

Subordinate monkeys exhibit behavior indicating higher psychological stress than dominant monkeys, and this is reflected by chronic high blood cortisol, visceral fat, and increased coronary artery disease risks in the subordinates [AMERICAN JOURNAL OF PRIMATOLOGY; Shively,CA; 71(9):742-751 (2009)]. A 15-year study of nurses aged 45-50 who reported pressure at work to be "much too high" had nearly twice the risk of developing ischemic heart disease as nurses who reported no stress — and nurses reporting pressure to be "a little too high" had 60% higher risk [OCCUPATIONAL AND ENVIRONMENTAL MEDICINE; Allesoe,K; 67(5):318-322 (2010)]. Physical activity or eating is more likely to precede myocardial infarction in men, whereas emotional stress is more likely to precede myocardial infarction in women [INTERNATIONAL JOURNAL OF CARDIOLOGY; Culic,V; 99(1):1-8 (2005)].

Subjects identified as highly anxious have been shown to have six times the risk of sudden cardiac death [ARCHIVES OF INTERNAL MEDICINE; Januzzi,JL; 160(13):1913-1921 (2000)]. Men aged 45-59 showing symptoms of psychological distress had more than triple the risk of fatal stroke [STROKE; May,M; 33(1):7-12 (2002)]. Men and women aged 48-67 identified as having high anger personalities had nearly triple the risk of stroke [STROKE; Williams,JE; 33(1):13-20 (2002)]. In a 10-15 year study of men, those in the lowest third for control has a 35% greater risk of cardiovascular disease, and those with the highest cynical distrust had 31% greater risk [PSYCHOSOMATIC MEDICINE; Haukkla,A; 72(6):556-562 (2010)]. Mortality is more than four times as great for coronary artery disease patients with high rather than low psychosocial stress, but exercise can substantially reduce mortality in patients who show a high change in exercise capacity after physical training [AMERICAN JOURNAL OF MEDICINE; Milani,RV; 122(10):931-938 (2009)].

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Mice subjected to chronic stress show impaired T-cell mediated immunity due to decreased thyroid hormone [BIOLOGICAL PSYCHIATRY; Frick,LR; 65(11):935-942 (2009)]. Psychological stress has been shown to decrease Natural Killer cell (NK cell) activity, decrease T lymphocytes, and reduce lymphocyte proliferation [CELLULAR IMMUNITY; Marketon,JI; 252(1-2):16-26 (2008)]. Female rats have been shown to have reduced NK cell activity during the phase of their estrous cycle characterized by high estradiol only if epinephrine (adrenaline) is also high [BRITISH JOURNAL OF CANCER; Ben-Eliyahu,S; 83(12):1747-1754 (2000)].

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A study of postmenopausal women showed that those with the highest levels of perceived psychological stress have leucocyte telomeres shortened by as much as would be expected from a decade of aging [PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES (USA); Epel,ES; 101(49):17312-17315 (2004)]. A similar study showed lower telomerase activity and higher epinephrine levels in women with high psychological stress [PSYCHONEUROENDOCRINOLOGY; Epel,ES; 31(3):277-287 (2006)]. Male and female patients with mood disorders believed to be associated with psychological stress were found to have considerably shorter telomeres than age-matched controls [BIOLOGICAL PSYCHIATRY; Simon,NM; 60(5):432-435 (2006)].

Subjects who participated in a 3-month mindfullness meditation retreat intended to reduce psychological stress showed nearly 30% greater leucocyte telomerase activity compared to controls [PSYCHONEUROENDOCRINOLOGY; Jacobs,TL; Oct 29 (2010)]. Similarly, exercise can protect against the telomere shortening associated with psychological stress [PLOS ONE; Puterman,E; 5(5):e10837 (2010)].

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Rats administered glucocorticoids show reduced neurogenesis in the dentate gyrus of the hippocampus [NEUROSCIENCE; Cameron,HA; 61(2):203-209 (1994)]. Rats subjected to a variety of stresses showed a reduction in neurogenesis that could be reversed by pharmaceutical glucocorticoid receptor blockade [EUROPEAN JOURNAL OF NEUROSCIENCE; Oomen,CA; 26(12):3395-3401 (2007)] and DeHydroEpiAndrosterone (DHEA) [NEUROSCIENCE; Kimonides,VG; 89(2):429-436 (1999)]. Tree shrews subjected to psychosocial stress (dominance by another shrew) show a retraction of hippocampal CA3 dendrites, but the retraction can be blocked by pharmacological inhibition of excitatory amino acids (which have been shown to act synergistically with glucocorticoids) [JOURNAL OF NEUROSCIENCE; Magarinos,AM; 16(10):3534-3540 (1996)]. Glucocorticoid administration to rats results in a loss of synapses, but not a loss of cells — and the effect is believed to be reversible [JOURNAL OF COMPARATIVE NEUROLOGY; Tata,DA; 498:363-374 (2006)]. Human victims of Post Traumatic Stress Disorder (PTSD, male war veterans) showed volume loss in the CA3/dentate gyrus, implicating chronic stress in suppressing neurogenesis [ARCHIVES OF GENERAL PSYCHIATRY; Wang,Z; 67(3):296-303 (2010)].

Rats subjected to learned helplessness conditioning (electric shocks) became desensitized to serotonin, but exercise (running) reduces this effect [JOURNAL OF NEUROSCIENCE; Greenwood,BN; 23(7):2889-2898 (2003)]. Depression of hippocampal neurogenesis by learned helplessness conditioning in rats can be reversed by the serotonin selective reuptake inhibitor fluoxetine (Prozac) [NEUROPSYCHOPHARMACOLOGY; Malberg,JE; 28(9):1562-1571 (2003)].

Newborn mice subjected to psychological stress (periodic infant-mother separation) show epigenetic changes resulting in sustained glucocorticoid sensitivity that is associated with impaired memory performance and stress-coping ability as adults [NATURE NEUROSCIENCE; Murgatroyd,C; 12(12):1559-1566 (2009)]. Healthy humans fed fish oil rich in the omega-3 fatty acids EPA and DHA show reduced plasma levels of the stress-associated hormone norepinephrine [NUTRITION; Hamazaki,K; 21(6):705-710 (2005)].

Healthy humans administered glucocorticoid (cortisol) in high doses comparable to cortisol levels induced by high psychological stress show reversible decrease in verbal declarative memory [ARCHIVES OF GENERAL PSYCHIATRY; Newcomer,JW; 56(6):527-533 (1999)]. Although high levels of glucocorticoid are associated with impaired memory in rats, low levels of glucocorticoid are also associated with impaired memory — intermediate levels give optimal memory performance [DOSE-RESPONSE; Park,CR; 4(1):55-74 (2006)]. This result is consistent with the Yerkes-Dodson law of motivational psychology which associates optimal performance with intermediate levels of anxiety. CRAN (Caloric Restriction with Adequate Nutrition) results in elevated glucocorticoid, but CRAN subjects do not suffer the normal deleterious effects of glucocorticoids on brain aging, apparently because of reduced oxidative damage, as well as increased neurotropic function and heat-shock proteins [NEUROBIOLOGY OF AGING; Patel,NV; 23(5):707-717 (2002)].

High levels of glucocorticoid (cortisol) enhances memory consolidation in association with high emotional stimulation from the amygdala, while simultaneously blocking memory retrieval [BRAIN RESEARCH; Wolf,OT; 1293:142-154 (2009)]. Melatonin enhances memory consolidation under stress [PSYCHOPHARMACOLOGY; Rimmele,U; 202(4):663-672 (2009)].

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