Lipid reactivity to stress: II. Biological and behavioral influences.

Stoney, Catherine M.; Bausserman, Linda; Niaura, Raymond; Marcus, Bess H.; Flynn, M. A. T.

doi:10.1037/0278-6133.18.3.251

Cited by 38 publications

(24 citation statements)

References 73 publications

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“…However, findings are inconsistent with some studies suggesting elevations in blood lipids even after adjustment for changes in hemoconcentration [18,19].…”

Section: Introductioncontrasting

confidence: 47%

Changes in plasma lipids with psychosocial stress are related to hypertension status and the norepinephrine stress response

et al. 2009

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Hypertension is a known risk factor for cardiovascular disease. Hypertensive individuals show exaggerated norepinephrine (NE) reactivity to stress. Norepinephrine is a known lipolytic factor. It is unclear if, in hypertensive individuals, stress-induced increases in NE are linked with the elevations in stress-induced circulating lipid levels. Such a mechanism could have implications for atherosclerotic plaque formation. In a cross-sectional, quasi-experimentally controlled study, 22 hypertensive and 23 normotensive men (mean +/-SEM, 45 +/-3 years) underwent an acute standardized psychosocial stress task combining public speaking and mental arithmetic in front of an audience. We measured plasma NE and the plasma lipid profile (total cholesterol [TC], low-density-lipoprotein cholesterol [LDL-C], high-density-lipoprotein cholesterol, and triglycerides) immediately before and after stress and at 20 and 60 minutes of recovery. All lipid levels were corrected for stress hemoconcentration. Compared with normotensives, hypertensives had greater TC (P = .030) and LDL-C (P = .037) stress responses. Independent of each other, mean arterial pressure (MAP) upon screening and immediate increase in NE predicted immediate stress change in TC (MAP: beta = .41, P = .003; NE: beta = .35, P = .010) and LDL-C (MAP: beta = .32, P = .024; NE: beta = .38, P = .008). Mean arterial pressure alone predicted triglycerides stress change (beta = .32, P = .043) independent of NE stress change, age, and BMI. The MAP-by-NE interaction independently predicted immediate stress change of high-density-lipoprotein cholesterol (beta = -.58, P < .001) and of LDL-C (beta = -.25, P < .08). We conclude that MAP and NE stress reactivity may elicit proatherogenic changes of plasma lipids in response to acute psychosocial stress, providing one mechanism by which stress might increase cardiovascular risk in hypertension.

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“…However, findings are inconsistent with some studies suggesting elevations in blood lipids even after adjustment for changes in hemoconcentration [18,19].…”

Section: Introductioncontrasting

confidence: 47%

Changes in plasma lipids with psychosocial stress are related to hypertension status and the norepinephrine stress response

et al. 2009

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“…However, no significant change in haematocrit was recorded in either experimental group. Other studies have recorded increases in haematocrit with severe, but not moderate, mental stress [33], and the stimuli utilized in the present study may not have been sufficiently intense to induce changes.…”

Section: Discussionmentioning

confidence: 49%

Acute mental stress elicits delayed increases in circulating inflammatory cytokine levels

et al. 2001

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The influence of acute mental stress on cardiovascular responses and concentrations of inflammatory cytokines up to 2 h later was assessed in 12 subjects exposed to stress and in eight control subjects. Beat-by-beat recordings of finger blood pressure and heart rate were made at rest and during two behavioural tasks (colour-word interference and mirror tracing). Blood was drawn after adaptation and at 45 min and 2 h after the tasks, and assayed for interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), interleukin-1 receptor antagonist (IL-1Ra), C-reactive protein (CRP) and haematocrit. Saliva was sampled periodically and assayed for free cortisol. The tasks were rated as stressful by the participants. The stress group showed significant increases in systolic and diastolic blood pressure (mean rises of 16.4p12.3 and 12.6p6.9 mmHg respectively) and heart rate (5.39p5.3 beats/min) ; these values returned to baseline during the recovery period. The IL-6 concentration was increased by 56 % at 2 h after the tasks (P 0.05), while IL1Ra was increased by 12.3 % (P 0.01). No changes in cardiovascular variables or cytokine concentrations were observed in the control subjects, and haematocrit did not change. The magnitude of blood pressure responses during tasks was correlated positively with the IL-6 concentration after 45 min (r l 0.70, P 0.05), and with the IL-1Ra concentration after 2 h (r l 0.63, P 0.05). Increases in TNF-α after 2 h were correlated with heart rate responses to tasks (r l 0.66, P 0.05). Associations between IL-6 and IL-1Ra concentrations were also recorded. This study indicates that inflammatory cytokines respond to acute mental stress in humans with delayed increases, and suggest that individual differences in cytokine responses are associated with sympathetic reactivity.

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“…Second, although acute stress was previously linked to serum cholesterol changes in humans [28, 29], our findings offer insight into early AS physiology that may promote stress-related CVD. That is, AS-related cardiovascular changes in ECS and FAE activity appear consistent with atherogenic inflammation and lipogenesis (e.g., elevated TAG) [30-32].…”

Section: Discussionmentioning

confidence: 86%

Effects of Acute Stress on Cardiac Endocannabinoids, Lipogenesis, and Inflammation in Rats

Holman

Guijarro

Lim

et al. 2014

Psychosomatic Medicine

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Objective Trauma exposure can precipitate acute/post-traumatic stress responses (AS/PTSD) and disabling cardiovascular disorders (CVD). Identifying acute stress-related physiologic changes that may increase CVD risk could inform development of early CVD-prevention strategies. The endocannabinoid system (ECS) regulates hypothalamic-pituitary-adrenal (HPA) axis response and stress-related cardiovascular function. We examine stress-related endocannabinoid system (ECS) activity and its association with cardiovascular biochemistry/function following acute stress. Methods Rodents (n=8-16/group) were exposed to predator odor or saline; elevated plus maze (EPM), blood pressure (BP), serum and cardiac tissue ECS markers, and lipid metabolism were assessed at 24h and 2wks post-exposure. Results At 24h the predator odor group demonstrated anxiety-like behavior and had (a) elevated serum markers of cardiac failure/damage (brain natriuretic peptide [BNP]: 275.1 vs. 234.6, p=0.007; troponin-I: 1.50 vs. 0.78, p=0.076), lipogenesis (triacylglycerols [TAG]: 123.5 vs. 85.93, p=0.018), and inflammation (stearoyl delta-9 desaturase activity [SCD-16]: 0.21 vs. 0.07, p<0.001); (b) significant decrease in cardiac endocannabinoid (2-arachidonoyl-sn-glycerol, 2-AG: 29.90 vs. 65.95, p<0.001) and fatty acid ethanolamides (FAE: oleoylethanolamide, OEA: 114.3 vs. 125.4, p=0.047; palmitoylethanolamide, PEA: 72.96 vs. 82.87, p=0.008); and (c) increased cardiac inflammation (IL-1β/IL-6 ratio: 19.79 vs.13.57, p=0.038; TNF-α/IL-6 ratio: 1.73 vs. 1.03, p=0.019) and oxidative stress (thiobarbituric acid reactive substances [TBARS]: 7.81 vs. 7.05, p=0.022), that were associated with cardiac steatosis (higher TAG: 1.09 vs. 0.72, p<0.001). Cardiac lipogenesis persisted, and elevated BP emerged two weeks after exposure. Conclusions Acute psychological stress elicits ECS-related cardiac responses associated with persistent, potentially-pathological changes in rat cardiovascular biochemistry/function.

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Lipid reactivity to stress: II. Biological and behavioral influences.

Cited by 38 publications

References 73 publications

Changes in plasma lipids with psychosocial stress are related to hypertension status and the norepinephrine stress response

Changes in plasma lipids with psychosocial stress are related to hypertension status and the norepinephrine stress response

Acute mental stress elicits delayed increases in circulating inflammatory cytokine levels

Effects of Acute Stress on Cardiac Endocannabinoids, Lipogenesis, and Inflammation in Rats

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