Health Psychology - CVD & CHD

Heart & CVD: Protective Factos

Protective Factors - Stress Management - CBT - Beta-Blockers - Fish Oil - Health Behavior Interventions - Social Relationships

Threat vs. Challenge

▪ when you view something as a threat you have a very different cardiovascular profile than you would if you viewed it as a challenge

Cardiovascular Disease

▪ ⅓ people suffer from hypertension What is blood pressure a consequence of? What could be increasing blood pressure? ▪ if there's more resistance, harder to get blood through those vessels, you are going to have higher blood pressure ▪ if there's a lot of force going through those blood vessels, over time there's more force on the blood vessels, they start to get more muscular & stronger to resist that force, and this actually creates more resistance - this can happen if you're constantly getting stressed

Does Stress Have Causal Effects on CHD?

▪ you get stressed out when your demands become too much for you to cope with them --> this method tries to help you reappraise stressors ******************************* Blumenthal et al 2016 Enhancing Cardiac Rehabilitation With Stress Management Training- A Randomized, Clinical Efficacy Trial - Circulation *BACKGROUND:* Cardiac rehabilitation (CR) is the standard of care for patients with coronary heart disease. Despite considerable epidemiological evidence that high stress is associated with worse health outcomes, stress management training (SMT) is not included routinely as a component of CR. *METHODS AND RESULTS:* One hundred fifty-one outpatients with coronary heart disease who were 36 to 84 years of age were randomized to 12 weeks of comprehensive CR or comprehensive CR combined with SMT (CR+SMT), with assessments of stress and coronary heart disease biomarkers obtained before and after treatment. A matched sample of CR-eligible patients who did not receive CR made up the no-CR comparison group. All participants were followed up for up to 5.3 years (median, 3.2 years) for clinical events. Patients randomized to CR+SMT exhibited greater reductions in composite stress levels compared with those randomized to CR alone (P=0.022), an effect that was driven primarily by improvements in anxiety, distress, and perceived stress. Both CR groups achieved significant, and comparable, improvements in coronary heart disease biomarkers. Participants in the CR+SMT group exhibited lower rates of clinical events compared with those in the CR-alone group (18% versus 33%; hazard ratio=0.49; 95% confidence interval, 0.25-0.95; P=0.035), and both CR groups had lower event rates compared with the no-CR group (47%; hazard ratio=0.44; 95% confidence interval, 0.27-0.71; P<0.001). *CONCLUSIONS:* CR enhanced by SMT produced significant reductions in stress and greater improvements in medical outcomes compared with standard CR. Our findings indicate that SMT may provide incremental benefit when combined with comprehensive CR and suggest that SMT should be incorporated routinely into CR. Stress Management Training Patients in the CR+SMT group received the identical comprehensive CR intervention plus SMT. SMT was adapted from our previous work,8,9 which combined education, group support, and cognitive-behavior therapy. The intervention was delivered in 12 weekly 1.5-hour sessions in groups of 4 to 8 participants. The SMT intervention is based on a cognitive-behavioral model in which stress is conceptualized as an imbalance between high demands (often environmental but also can be self-imposed) and more limited coping resources. Therefore, the intervention is directed at reducing demands and increasing coping abilities. The initial sessions are designed to establish rapport, to promote group cohesion and social support, and to provide a scientific basis for the importance of stress as a risk factor for adverse cardiovascular events. Strategies for reducing demands, including prioritizing, time management, establishing personal values, and avoiding stress-producing situations, are presented. Subsequent sessions focus on modifying responses to situations that cannot be readily changed. Several sessions are devoted to training in progressive muscle relaxation techniques and the use of visual imagery to reduce stress. Emphasis is placed on the importance of cognitive appraisals in affecting stress responses, with recognition of irrational beliefs and cognitive distortions such as overgeneralization, catastrophizing, and all-or-nothing thinking. Later sessions focus on the importance of effective communication, including topics of assertiveness and anger management. Instruction in problem-solving strategies is also provided in which participants are encouraged to apply the skills that they have learned to address everyday problems. Methods included brief lectures, group discussion, role playing, instruction in specific behavioral skills, and weekly homework assignments.

Omega-3 Fatty Acids: Summary

*fish oils may counteract the fats (from your cheeseburgers and fries) that can actually increase inflammation*

Heart & CVD : Risk Factors

- Demographics (Sex &Ethnicity) - Inflammation (e.g. CRP) - Depression - Stress - Social Isolation - Work Stress - Emotional & Personality Factors: - Type A - Hostility

Basic Processes Related to Diseases of the Heart

- Hypertension - Atherosclerosis - Type II Diabetes

From Time Magazine: Atherosclerosis and CRP

Ask any heart doctor the best way to avoid a heart attack, and he will probably tell you to lower your cholesterol and exercise more. What he's not likely to tell you is that despite cholesterol's well-earned reputation as the heart's primary nemesis, half of all heart attacks occur in people with normal cholesterol levels. That's because though scientists have identified some 250 other risk factors, from obesity to gum disease, they have never found a better indicator of the health of one's cardiovascular system than the levels of good and bad cholesterol in the blood. Until now. In a groundbreaking study published in the New England Journal of Medicine last week, doctors from Boston's Brigham and Women's Hospital showed that a simple blood test, called CRP, that measures the presence and intensity of inflammation in the walls of the blood vessels is as good as and in some cases better than cholesterol levels at predicting which patients are most likely to suffer a heart attack or stroke. The study, led by Dr. Paul Ridker, director of the hospital's center for cardiovascular-disease prevention, is likely to be the talk of the annual meeting of the American Heart Association this week in Chicago. Not only does it provide the strongest evidence to date that inflammation plays a key role in heart disease, but it also supports the growing suspicion among medical researchers that inflammation is a major culprit behind a wide range of disorders, including cancer. Inflammation is the body's basic emergency-response system. When anything threatens the body's health--from disease-causing germs to the buildup of fatty plaque in the walls of a heart vessel--the immune system sends in wave after wave of cells to swarm and destroy the invader. In the blood vessels, layers of these immune cells pile up, creating lesions that become increasingly unstable and may eventually rupture, triggering a heart attack. How sensitive this alarm system is depends on such things as diet, stress and one's genetic predisposition. CRP, for C-reactive protein, is a substance manufactured by the liver in response to the immune system's alarms. It can easily be picked up in the blood and provides a convenient measure of how inflamed the heart arteries may be. Ridker's team, which pioneered the study of CRP's role in heart disease, tracked the levels of both CRP and LDL ("bad" cholesterol) in nearly 28,000 women for eight years. They found that women with high levels of CRP were twice as likely to have heart disease as those with high LDL, and that many women who later suffered heart attacks would have been given a clean bill of health on the basis of their low LDLs. For that reason, he and others would like to see CRP join cholesterol as part of the battery of tests in a standard blood workup. "These data," says Ridker, "tell us that continued reliance on LDL alone is really not serving our purpose very well." But CRP can be tricky; it can jump as much as 10-fold when a person is fighting a cold or the flu. And it shouldn't be used in place of a cholesterol test. The latter measures how much fat is lodged in the vessels of the heart; the CRP test shows how likely it is that those plaques will burst. If your CRP levels are high, don't despair. They can be lowered. In fact, the lifestyle changes and medications that doctors recommend to lower cholesterol do double duty and also reduce CRP. Avoiding fatty red meat, eating more fruits and vegetables and exercising should be the first response--if making those changes is not enough, statin drugs may help. The broader implications of the new study will require further research. People who suffer from chronic inflammatory responses like arthritis may be at higher risk of heart disease. There may also be a cancer link, for among the substances released during the inflammatory response are free radicals that can trigger tumor growth. Maybe that's why doctors' advice to eat more nutrient-rich vegetables and less fat works equally well for a patient who is at risk for cancer or for heart disease. They've been treating the same underlying cause all along.

Work Stress & CHD

Boehm, J. K., & Kubzansky, L. D. (2012). The heart's content: The association between positive psychological well-being and cardiovascular health. Psychological Bulletin, 138, 655-691. doi:10.1037/a0027448

BP Reactivity & CVD Mortality

Carroll et al Phillips 2012 Increased blood pressure reactions to acute mental stress are associated with 16-year cardiovascular disease mortality - Psychophys Exaggerated cardiovascular reactions to acute psychological stress may be involved in the etiology of cardiovascular pathology. The present analysis examined the association between the magnitude of systolic and diastolic blood pressure reactions to stress and cardiovascular disease mortality. Participants were 431 (229 women) from the West of Scotland Twenty-07 Study, aged 63 years at the time of stress testing, where blood pressure was measured during resting baseline and mental arithmetic stress. Participants' vital status was tracked for the next 16 years, during which time 38 had died of cardiovascular disease. Both systolic and diastolic blood pressure reactions were positively associated with cardiovascular disease mortality. This association could reflect the long-term erosive effects of exaggerated reactivity on the vasculature as well as its short-term capacity to trigger acute cardiovascular events.

Diabetes Prevention - Part 2

Diabetes Prevention Research Group 2002 Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin - NEJM Background Type 2 diabetes affects approximately 8 percent of adults in the United States. Some risk factors — elevated plasma glucose concentrations in the fasting state and after an oral glucose load, overweight, and a sedentary lifestyle — are potentially reversible. We hypothesized that modifying these factors with a lifestyle-intervention program or the administration of metformin would prevent or delay the development of diabetes. Methods We randomly assigned 3234 nondiabetic persons with elevated fasting and post-load plasma glucose concentrations to placebo, metformin (850 mg twice daily), or a lifestyle-modification program with the goals of at least a 7 percent weight loss and at least 150 minutes of physical activity per week. The mean age of the participants was 51 years, and the mean body-mass index (the weight in kilograms divided by the square of the height in meters) was 34.0; 68 percent were women, and 45 percent were members of minority groups. Results The average follow-up was 2.8 years. The incidence of diabetes was 11.0, 7.8, and 4.8 cases per 100 person-years in the placebo, metformin, and lifestyle groups, respectively. The lifestyle intervention reduced the incidence by 58 percent (95 percent confidence interval, 48 to 66 percent) and metformin by 31 percent (95 percent confidence interval, 17 to 43 percent), as compared with placebo; the lifestyle intervention was significantly more effective than metformin. To prevent one case of diabetes during a period of three years, 6.9 persons would have to participate in the lifestyle-intervention program, and 13.9 would have to receive metformin. Conclusions Lifestyle changes and treatment with metformin both reduced the incidence of diabetes in persons at high risk. The lifestyle intervention was more effective than metformin. (N Engl J Med 2002; 346:393-403.)

Effects of Intervention on CRP

Diabetes Prevention Research Group 2005 Intensive lifestyle intervention or metformin on inflammation and coagulation in participants with impaired glucose tolerance. - Diabetes Increases in subclinical inflammation (C-reactive protein [CRP]) and impaired coagulation have been associated with increased obesity and insulin resistance. Only a few small studies have examined the effect of lifestyle changes, such as weight loss, increased physical activity, and insulin-sensitizing intervention on inflammation and coagulation. The Diabetes Prevention Program (DPP) clinical trial studied the effect of an intensive lifestyle intervention or metformin on progression to diabetes relative to placebo in 3,234 adults with impaired glucose tolerance. The effects of these interventions on CRP and fibrinogen at 12 months are examined in this report. Metformin reduced CRP in women compared with the placebo group. In men, the median changes in CRP from baseline to 1 year were -33% in the lifestyle group, -7% in the metformin group, and +5% in the placebo group. In women, the changes in CRP from baseline to follow-up were -29% in the lifestyle group, -14% in the metformin group, and 0% in the placebo group. In the lifestyle group weight loss rather than increased physical activity seems to account for most of the changes in CRP. Only modest reductions (although significant) were seen in fibrinogen levels in the lifestyle group relative to the metformin and placebo group. Lifestyle intervention reduced levels of nontraditional cardiovascular risk factors relative to both placebo and to a lesser degree to metformin.

C-Reactive Protein (CRP) and Diseases of the Heart

Emerging Risk Factors Collaboration 2010 C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality- an individual participant meta-analysis - Lancet Background Associations of C-reactive protein (CRP) concentration with risk of major diseases can best be assessed by long-term prospective follow-up of large numbers of people. We assessed the associations of CRP concentration with risk of vascular and non-vascular outcomes under diff erent circumstances. Methods We meta-analysed individual records of 160 309 people without a history of vascular disease (ie, 1.31 million person-years at risk, 27 769 fatal or non-fatal disease outcomes) from 54 long-term prospective studies. Within-study regression analyses were adjusted for within-person variation in risk factor levels. Results Loge CRP concentration was linearly associated with several conventional risk factors and infl ammatory markers, and nearly log-linearly with the risk of ischaemic vascular disease and non-vascular mortality. Risk ratios (RRs) for coronary heart disease per 1-SD higher loge CRP concentration (three-fold higher) were 1.63 (95% CI 1.51-1.76) when initially adjusted for age and sex only, and 1.37 (1.27-1.48) when adjusted further for conventional risk factors; 1.44 (1.32-1.57) and 1.27 (1.15-1.40) for ischaemic stroke; 1.71 (1.53-1.91) and 1.55 (1.37-1.76) for vascular mortality; and 1.55 (1.41-1.69) and 1.54 (1.40-1.68) for non-vascular mortality. RRs were largely unchanged after exclusion of smokers or initial follow-up. After further adjustment for fi brinogen, the corresponding RRs were 1.23 (1.07-1.42) for coronary heart disease; 1.32 (1.18-1.49) for ischaemic stroke; 1.34 (1.18-1.52) for vascular mortality; and 1.34 (1.20-1.50) for non-vascular mortality. Interpretation CRP concentration has continuous associations with the risk of coronary heart disease, ischaemic stroke, vascular mortality, and death from several cancers and lung disease that are each of broadly similar size. The relevance of CRP to such a range of disorders is unclear. Associations with ischaemic vascular disease depend considerably on conventional risk factors and other markers of infl ammation.

Fish Consumption and Cardiovascular Disease

Epidemiological Studies of Diet: - Increased consumption of fish associated with lower risk of coronary heart disease (meta-analysis with 222,364 individuals) - Eating fish once per week, leads to a 15% reduction in CHD risk ****************************************************** He, K., et al. "Accumulated evidence on fish consumption and coronary heart disease mortality: a meta-analysis of cohort studies." Circulation, v. 109 issue 22, 2004, p. 2705-11. *Background* —Results from observational studies on fish consumption and coronary heart disease (CHD) mortality are inconsistent. *Methods and Results* —A meta-analysis of cohort studies was conducted to examine the association between fish intake and CHD mortality. Studies were included if they provided a relative risk (RR) and corresponding 95% CI for CHD mortality in relation to fish consumption and the frequency of fish intake. A database was developed on the basis of 11 eligible studies and 13 cohorts, including 222 364 individuals with an average 11.8 years of follow-up. Pooled RR and 95% CI for CHD mortality were calculated by using both fixed-effect and random-effect models. A linear regression analysis of the log RR weighted by the inverse of variance was performed to assess the possible dose-response relation. Compared with those who never consumed fish or ate fish less than once per month, individuals with a higher intake of fish had lower CHD mortality. The pooled multivariate RRs for CHD mortality were 0.89 (95% CI, 0.79 to 1.01) for fish intake 1 to 3 times per month, 0.85 (95% CI, 0.76 to 0.96) for once per week, 0.77 (95% CI, 0.66 to 0.89) for 2 to 4 times per week, and 0.62 (95% CI, 0.46 to 0.82) for 5 or more times per week. Each 20-g/d increase in fish intake was related to a 7% lower risk of CHD mortality (P for trend_0.03). *Conclusions* —These results indicate that fish consumption is inversely associated with fatal CHD. Mortality from CHD may be reduced by eating fish once per week or more.

Laboratory Stress Response Predicts Future Resting Blood Pressure

Flaa, Eide, Kjeldsen, Rostrup 2008 Sympathoadrenal Stress Reactivity Is a Predictor of Future Blood Pressure An 18-Year Follow-Up Study - Hypertension

Risk Factors for Heart Attack

From Steptoe & Kivimaki 2012 Stress & Cardiovascular Disease - Nat Rev Cardio Yusuf et al 2004 Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study)- case-control study - Lancet *BACKGROUND:* Although more than 80% of the global burden of cardiovascular disease occurs in low-income and middle-income countries, knowledge of the importance of risk factors is largely derived from developed countries. Therefore, the effect of such factors on risk of coronary heart disease in most regions of the world is unknown. *METHODS:* We established a standardised case-control study of acute myocardial infarction in 52 countries, representing every inhabited continent. 15152 cases and 14820 controls were enrolled. The relation of smoking, history of hypertension or diabetes, waist/hip ratio, dietary patterns, physical activity, consumption of alcohol, blood apolipoproteins (Apo), and psychosocial factors to myocardial infarction are reported here. Odds ratios and their 99% CIs for the association of risk factors to myocardial infarction and their population attributable risks (PAR) were calculated. *FINDINGS:* Smoking (odds ratio 2.87 for current vs never, PAR 35.7% for current and former vs never), raised ApoB/ApoA1 ratio (3.25 for top vs lowest quintile, PAR 49.2% for top four quintiles vs lowest quintile), history of hypertension (1.91, PAR 17.9%), diabetes (2.37, PAR 9.9%), abdominal obesity (1.12 for top vs lowest tertile and 1.62 for middle vs lowest tertile, PAR 20.1% for top two tertiles vs lowest tertile), psychosocial factors (2.67, PAR 32.5%), daily consumption of fruits and vegetables (0.70, PAR 13.7% for lack of daily consumption), regular alcohol consumption (0.91, PAR 6.7%), and regular physical activity (0.86, PAR 12.2%), were all significantly related to acute myocardial infarction (p<0.0001 for all risk factors and p=0.03 for alcohol). These associations were noted in men and women, old and young, and in all regions of the world. Collectively, these nine risk factors accounted for 90% of the PAR in men and 94% in women. *INTERPRETATION:* Abnormal lipids, smoking, hypertension, diabetes, abdominal obesity, psychosocial factors, consumption of fruits, vegetables, and alcohol, and regular physical activity account for most of the risk of myocardial infarction worldwide in both sexes and at all ages in all regions. This finding suggests that approaches to prevention can be based on similar principles worldwide and have the potential to prevent most premature cases of myocardial infarction.

Depression & Heart Disease

Gan et al 2014 Depression and the risk of coronary heart disease- a meta-analysis of prospective cohort studies - BMC Psychiatry *Background* Several systematic reviews and meta-analyses demonstrated the association between depression and the risk of coronary heart disease (CHD), but the previous reviews had some limitations. Moreover, a number of additional studies have been published since the publication of these reviews. We conducted an updated meta-analysis of prospective studies to assess the association between depression and the risk of CHD. *Methods* Relevant prospective studies investigating the association between depression and CHD were retrieved from the PubMed, Embase, Web of Science search (up to April 2014) and from reviewing reference lists of obtained articles. Either a random-effects model or fixed-effects model was used to compute the pooled risk estimates when appropriate. *Results* Thirty prospective cohort studies with 40 independent reports met the inclusion criteria. These groups included 893,850 participants (59,062 CHD cases) during a follow-up duration ranging from 2 to 37 years. The pooled relative risks (RRs) were 1.30 (95% CI, 1.22-1.40) for CHD and 1.30 (95% CI, 1.18-1.44) for myocardial infarction (MI). In the subgroup analysis by follow-up duration, the RR of CHD was 1.36 (95% CI, 1.24-1.49) for less than 15 years follow-up, and 1.09 (95% CI, 0.96-1.23) for equal to or more than 15 years follow-up. Potential publication bias may exist, but correction for this bias using trim-and-fill method did not alter the combined risk estimate substantially. *Conclusions* The results of our meta-analysis suggest that depression is independently associated with a significantly increased risk of CHD and MI, which may have implications for CHD etiological research and psychological medicine. Pan et al 2011 Depression and risk of stroke morbidity and mortality a meta-analysis and systematic review - JAMA.pdf *CONTEXT:* Several studies have suggested that depression is associated with an increased risk of stroke; however, the results are inconsistent. *OBJECTIVE:* To conduct a systematic review and meta-analysis of prospective studies assessing the association between depression and risk of developing stroke in adults. *DATA SOURCES:* A search of MEDLINE, EMBASE, and PsycINFO databases (to May 2011) was supplemented by manual searches of bibliographies of key retrieved articles and relevant reviews. *STUDY SELECTION:* We included prospective cohort studies that reported risk estimates of stroke morbidity or mortality by baseline or updated depression status assessed by self-reported scales or clinician diagnosis. *DATA EXTRACTION:* Two independent reviewers extracted data on depression status at baseline, risk estimates of stroke, study quality, and methods used to assess depression and stroke. Hazard ratios (HRs) were pooled using fixed-effect or random-effects models when appropriate. Associations were tested in subgroups representing different participant and study characteristics. Publication bias was evaluated with funnel plots and Begg test. *RESULTS:* The search yielded 28 prospective cohort studies (comprising 317,540 participants) that reported 8478 stroke cases (morbidity and mortality) during a follow-up period ranging from 2 to 29 years. The pooled adjusted HRs were 1.45 (95% CI, 1.29-1.63; P for heterogeneity <.001; random-effects model) for total stroke, 1.55 (95% CI, 1.25-1.93; P for heterogeneity = .31; fixed-effects model) for fatal stroke (8 studies), and 1.25 (95% CI, 1.11-1.40; P for heterogeneity = .34; fixed-effects model) for ischemic stroke (6 studies). The estimated absolute risk differences associated with depression were 106 cases for total stroke, 53 cases for ischemic stroke, and 22 cases for fatal stroke per 100,000 individuals per year. The increased risk of total stroke associated with depression was consistent across most subgroups. *CONCLUSION:* Depression is associated with a significantly increased risk of stroke morbidity and mortality. Lichtman et al 2014 Depression as a risk factor for poor prognosis among patients with acute coronary syndrome- systematic review and recommendations- a scientific statement from the American Heart Association - Circulation *BACKGROUND:* Although prospective studies, systematic reviews, and meta-analyses have documented an association between depression and increased morbidity and mortality in a variety of cardiac populations, depression has not yet achieved formal recognition as a risk factor for poor prognosis in patients with acute coronary syndrome by the American Heart Association and other health organizations. The purpose of this scientific statement is to review available evidence and recommend whether depression should be elevated to the status of a risk factor for patients with acute coronary syndrome. *METHODS AND RESULTS:* Writing group members were approved by the American Heart Association's Scientific Statement and Manuscript Oversight Committees. A systematic literature review on depression and adverse medical outcomes after acute coronary syndrome was conducted that included all-cause mortality, cardiac mortality, and composite outcomes for mortality and nonfatal events. The review assessed the strength, consistency, independence, and generalizability of the published studies. A total of 53 individual studies (32 reported on associations with all-cause mortality, 12 on cardiac mortality, and 22 on composite outcomes) and 4 meta-analyses met inclusion criteria. There was heterogeneity across studies in terms of the demographic composition of study samples, definition and measurement of depression, length of follow-up, and covariates included in the multivariable models. Despite limitations in some individual studies, our review identified generally consistent associations between depression and adverse outcomes. *CONCLUSIONS:* Despite the heterogeneity of published studies included in this review, the preponderance of evidence supports the recommendation that the American Heart Association should elevate depression to the status of a risk factor for adverse medical outcomes in patients with acute coronary syndrome.

Social Isolation, CRP, & CHD

Heffner et al 2011 Social isolation, C-reactive protein, and coronary heart disease mortality among community-dwelling adults - Soc Sci Med Social isolation confers increased risk for coronary heart disease (CHD) events and mortality. In two recent studies, low levels of social integration among older adults were related to higher levels of C-reactive protein (CRP), a marker of inflammation, suggesting a possible biological link between social isolation and CHD. The current study examined relationships among social isolation, CRP, and 15-year CHD death in a community sample of US adults aged 40 years and older without a prior history of myocardial infarction. A nested case-cohort study was conducted from a parent cohort of community-dwelling adults from the southeastern New England region of the United States (N = 2321) who were interviewed in 1989 and 1990. CRP levels were measured from stored sera provided by the nested case-cohort (n = 370), which included all cases of CHD death observed through 2005 (n = 48), and a random sample of non-cases. We found that the most socially isolated individuals had two-and-a-half times the odds of elevated CRP levels compared to the most socially integrated. In separate logistic regression models, both social isolation and CRP predicted later CHD death. The most socially isolated continued to have more than twice the odds of CHD death compared to the most socially integrated in a model adjusting for CRP and more traditional CHD risk factors. The current findings support social isolation as an independent risk factor of both high levels of CRP and CHD death in middle-aged adults without a prior history of myocardial infarction. Prospective study of inflammatory pathways related to social isolation and mortality are needed to fully delineate whether and how CRP or other inflammatory markers contribute to mechanisms linking social isolation to CVD health.

Type A Personality: Graph

Higher pace of life associated with higher CHD disease

Does Stress Have Causal Effects on CHD? - Graph

Intervention reduced Clinical Events (all-cause mortality, myocardial infarction, stroke, angina ▪ Intervention had small, but significant effects on reducing anxiety and perceived stress, smaller effects on anger *causal evidence that reducing stress reduces cardiovascular disease* ********************************************************** *Figure 2.* Cumulative time-to-event curves for clinical events in the cardiac rehabilitation enhanced with stress management training (CR+SMT), cardiac rehabilitation only (CR-alone), and no-CR groups. Clinical events included all-cause mortality, myocardial infarction, cardiac or peripheral vascular intervention, stroke/transient ischemic attack, or unstable angina requiring hospitalization. Participants in the CR+SMT group were at significantly lower risk of clinical events compared with those in the CR-alone group (hazard ratio [HR]=0.47; 95% confidence interval [CI], 0.24-0.91; P=0.025). Both CR groups had lower event rates compared with a nonrandomized, matched no-CR control group (HR=0.35; 95% CI, 0.22-0.56; P<0.001). Number at risk represents participants with follow-up data for clinical events who had not yet had an event at years 0, 2, and 4.

Social Relationships, Oxytocin & Stroke

Karelina et al DeVries 2009 Social isolation alters neuroinflammatory response to stroke - PNAS Social isolation has dramatic long-term physiological and psychological consequences; however, the mechanisms by which social isolation influences disease outcome are largely unknown. The purpose of the present study was to investigate the effects of social isolation on neuronal damage, neuroinflammation, and functional outcome after focal cerebral ischemia. Male mice were socially isolated (housed individually) or pair housed with an ovariectomized female before induction of stroke, via transient intraluminal middle cerebral artery occlusion (MCAO), or SHAM surgery. In these experiments, peri-ischemic social isolation decreases poststroke survival rate and exacerbates infarct size and edema development. The social influence on ischemic damage is accompanied by an altered neuroinflammatory response; specifically, central interleukin-6 (IL-6) signaling is down-regulated, whereas peripheral IL-6 is up-regulated, in isolated relative to socially housed mice. In addition, intracerebroventricular injection of an IL-6 neutralizing antibody (10 ng) eliminates social housing differences in measures of ischemic outcome. Taken together, these data suggest that central IL-6 is an important mediator of social influences on stroke outcome.

Social Relationships, Oxytocin & Stroke - Part 2

Karelina, Stuller, Jarrett, Zhang, Wells, Norman, DeVries 2011 Oxytocin Mediates Social Neuroprotection After Cerebral Ischemia - Stroke Background and Purpose—The reduced incidence, morbidity, and mortality of stroke among humans with strong social support have been well-documented; however, the mechanisms underlying these socially mediated phenomena remain unknown, but may involve oxytocin (OT), a hormone that modulates some aspects of social behavior in humans and other animals. Methods—In the present study, adult male mice were socially isolated (housed individually) or socially paired (housed with an ovariectomized female); social pairing increased hypothalamic OT gene expression. To determine whether a causal relationship exists between increased OT and improved stroke outcome, mice were treated with exogenous OT or OT receptor antagonist beginning 1 week before induction of experimental stroke via middle cerebral artery occlusion. Results—Relative to social isolation, social housing attenuated infarct size, neuroinflammation, and oxidative stress following experimental stroke; the neuroprotective effect of social housing was eliminated by receptor antagonist treatment. In contrast, administration of OT to socially isolated mice reproduced the neuroprotection conferred by social housing. We further report evidence for a direct suppressive action of OT on cultured microglia, which is a key instigator in the development of neuroinflammation after cerebral ischemia. Conclusions—These findings support the hypothesis that OT mediates the neuroprotective effect of social interaction on stroke outcome

Omega-3's, Exam Stress, & Inflammation

Kiecolt-Glaser, Belury, Andridge, Malarkey, Glaser 2011 Kiecolt-Glaser, JK., et al. "Omega-3 supplementation lowers inflammation and anxiety in medical students- a randomized controlled trial." BBI v. 25 issue 8, 2011, p. 1725-34. Observational studies have linked lower omega-3 (n-3) polyunsaturated fatty acids (PUFAs) and higher omega-6 (n-6) PUFAs with inflammation and depression, but randomized controlled trial (RCT) data have been mixed. To determine whether n-3 decreases proinflammatory cytokine production and depressive and anxiety symptoms in healthy young adults, this parallel group, placebo-controlled, double-blind 12- week RCT compared n-3 supplementation with placebo. The participants, 68 medical students, provided serial blood samples during lower-stress periods as well as on days before an exam. The students received either n-3 (2.5 g/d, 2085 mg eicosapentaenoic acid and 348 mg docosahexanoic acid) or placebo capsules that mirrored the proportions of fatty acids in the typical American diet. Compared to controls, those students who received n-3 showed a 14% decrease in lipopolysaccharide (LPS) stimulated interleukin 6 (IL-6) production and a 20% reduction in anxiety symptoms, without significant change in depressive symptoms. Individuals differ in absorption and metabolism of n-3 PUFA supplements, as well as in adherence; accordingly, planned secondary analyses that used the plasma n-6:n-3 ratio in place of treatment group showed that decreasing n-6:n-3 ratios led to lower anxiety and reductions in stimulated IL-6 and tumor necrosis factor alpha (TNF-a) production, as well as marginal differences in serum TNF-a. These data suggest that n-3 supplementation can reduce inflammation and anxiety even among healthy young adults. The reduction in anxiety symptoms associated with n-3 supplementation provides the first evidence that n-3 may have potential anxiolytic benefits for individuals without an anxiety disorder diagnosis. ClinicalTrials.gov identifier: NCT00519779.

Hostility and Inflammation: Cross-cultural Differences?

Kitayama et al Coe 2015 Expression of Anger and Ill Health in Two Cultures- An Examination of Inflammation and Cardiovascular Risk - Psych Science Expression of anger is associated with biological health risk (BHR) in Western cultures. However, recent evidence documenting culturally divergent functions of the expression of anger suggests that its link with BHR may be moderated by culture. To test this prediction, we examined large probability samples of both Japanese and Americans using multiple measures of BHR, including pro-inflammatory markers (interleukin-6 and C-reactive protein) and indices of cardiovascular malfunction (systolic blood pressure and ratio of total to HDL cholesterol). We found that the link between greater expression of anger and increased BHR was robust for Americans. As predicted, however, this association was diametrically reversed for Japanese, among whom greater expression of anger predicted reduced BHR. These patterns were unique to the expressive facet of anger and remained after we controlled for age, gender, health status, health behaviors, social status, and reported experience of negative emotions. Implications for sociocultural modulation of bio-physiological responses are discussed.

Type A Personality: Is there a relationship between pace of life in America and CHD?

Levine et al 1989 The Type A city- Coronary heart disease and the pace of life - Jnl of Behav Med The relationship between the pace of life and coronary heart disease (CHD) was examined in a total of 36 small, medium, and large metropolitan areas across the United States. Four indicators of pace were observed: walking speed, articulation rate (talking speed), bank teller speed (work speed), and the proportion of individuals wearing watches (concern with clock time). Pace of life was strongly related to death rates from coronary heart disease both across cities and across regions of the country. This provides support, on a sociological level, for Wright's (1988) contention that time urgency is a toxic element of the Type A behavior pattern. It is proposed that individuals living in fast-paced cities may be more prone to unhealthy behaviors (e.g., cigarette smoking), which place them at a greater risk for CHD. The relationship among cities" temporal norms, Type A time urgency, and coronary heart disease is also discussed.

Metabolic Syndrome

Metabolic Syndrome = group of risk factors that greatly increase risk for CHD, stroke, and diabetes. Meet criteria for metabolic syndrome if have any three of the following five risk factors: 1. High Blood Pressure 2. Obesity, particularly at the waist line 3. High blood glucose (e.g. sugar) 4. Low levels of HDL ("Good" cholesterol) 5. High levels of lipids in blood (related to "bad" cholesterol *metabolic syndrome is when someone has 3 of those 5 risk factors

Fish Oil and Cardiovascular Disease

Mozaffarian & Wu 2011 Omega-3 Fatty acids and cardiovascular disease- effects on risk factors, molecular pathways, and clinical events." Journal of the American College of Cardiology

Hostility and Inflammation: Cross-cultural Differences? - graph

Relationship holds when control for health status and socioeconomic status Potential Explanation: To express anger outward in Japan you are likely of higher status and with greater power, while in U.S. may reflect exposure to negative events

Hostility Scale

Subsequent research has shown that the effects attributed to Type A behavior are driven by the Hostility component

Twitter, Hostility, & CHD - Graph

if you only use twitter, it is a HUGE predictor

Coronary Heart Disease

illnesses caused by atherosclerosis - #1 Killer in the USA = ~ 20% of all deaths

Hostility and Inflammation

• Relationship of self-reported hostility and inflammation studied in 856 health middle-aged adults ****************************************************************************** Marsland et al 2008 Antagonistic characteristics are positively associated with inflammatory markers independently of trait negative emotionality - BBI Recent evidence suggests that individuals with certain personality traits are at elevated risk for chronic systemic inflammation. To date, this literature has focused on the related traits of hostility and negative affect (NA). In this study, we examine the covariation of trait measures of hostility and NA with the inflammatory mediators interleukin-6 and C-reactive protein. We also explore whether observed associations reflect independent contributions of cognitive, affective and behavioral components of hostile dispositions or shared trait variance with global negative affectivity. Subjects were a diverse sample of 855 relatively healthy middle-aged community volunteers (50% male) from the Adult Health and Behavior Project. The Buss and Perry Aggression Questionnaire (BPAQ) and an Abbreviated Cook-Medley Hostility Scale (ACM) were used to measure dimensions of hostility, and the Multidimensional Personality Questionnaire was used to measure trait NA. Regression analyses accounting for demographic characteristics and medical covariates showed a positive relationship of all components of hostility and trait NA with both IL-6 and CRP. After controlling for trait NA, only the behavioral component of hostility was independently associated with the inflammatory markers. The relationships of cognitive and affective components of hostility with inflammatory markers were largely explained by lifestyle factors, particularly body mass index and smoking. In contrast, lifestyle factors did not explain the covariation of hostile behavioral tendencies and inflammation. These findings suggest that unique attributes of aggressive behavioral tendencies account for much of the variability in inflammation associated with hostility and negative emotions, raising the possibility that individuals high in aggression are at increased risk of inflammatory disease

Hostility and Mortality

▪ Hostility inventory given to 128 law students at UNC in 1956 ▪ Mortality follow-up done in 1985 ********************************************************** Barefoot, Dodge, PEterson, Dahlstrom, Williams 1989 The Cook-Medley hostility scale- item content and ability to predict survival - PM Previous studies have identified the MMPI-based Cook and Medley hostility scale (Ho) as a predictor of health outcomes. To achieve a better understanding of the construct measured by this scale, Ho items were classified on an a priori basis. Six subsets were identified: Cynicism, Hostile Attributions, Hostile Affect, Aggressive Responding, Social Avoidance, and Other. Study 1 examined the correlations of these subsets with scales of the NEO Personality Inventory in two samples of undergraduates. Good convergent and discriminant validity were demonstrated, but there was some evidence that items in the Social Avoidance and Other categories reflect constructs other than hostility. Study 2 examined the ability of the Ho scale and the item subsets to predict the 1985 survival of 118 lawyers who had completed the MMPIin 1956 and 1957. As in previous studies, those with high scores had poorer survival (x2 = 6.37, p = 0.012). Unlike previous studies, the relation between Ho scores and survival was linear. Cynicism, Hostile Affect, and Aggressive Responding subsets were related to survival, whereas the other subsets were not. The sum of the three predictive subsets, with a x2 of 9.45 (p = 0.002), was a better predictor than the full Ho scale, suggesting that it may be possible to refine the scale and achieve an even more effective measure of those aspects of hostility that are deleterious to health.

Atherosclerosis

▪ Inflammation drives all phases of atherosclerosis, including initiation, progression, and the eventual breaking off of the plaque that leads to a heart attack

Diabetes Prevention

▪ some of the drop on this graph was due to diet and exercise reducing weight - See page 272. Diabetes Prevention Research Group 2002 Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin - NEJM *Background* Type 2 diabetes affects approximately 8 percent of adults in the United States. Some risk factors — elevated plasma glucose concentrations in the fasting state and after an oral glucose load, overweight, and a sedentary lifestyle — are potentially reversible. We hypothesized that modifying these factors with a lifestyle-intervention program or the administration of metformin would prevent or delay the development of diabetes. *Methods* We randomly assigned 3234 nondiabetic persons with elevated fasting and post-load plasma glucose concentrations to placebo, metformin (850 mg twice daily), or a lifestyle-modification program with the goals of at least a 7 percent weight loss and at least 150 minutes of physical activity per week. The mean age of the participants was 51 years, and the mean body-mass index (the weight in kilograms divided by the square of the height in meters) was 34.0; 68 percent were women, and 45 percent were members of minority groups. *Results* The average follow-up was 2.8 years. The incidence of diabetes was 11.0, 7.8, and 4.8 cases per 100 person-years in the placebo, metformin, and lifestyle groups, respectively. The lifestyle intervention reduced the incidence by 58 percent (95 percent confidence interval, 48 to 66 percent) and metformin by 31 percent (95 percent confidence interval, 17 to 43 percent), as compared with placebo; the lifestyle intervention was significantly more effective than metformin. To prevent one case of diabetes during a period of three years, 6.9 persons would have to participate in the lifestyle-intervention program, and 13.9 would have to receive metformin. *Conclusions* Lifestyle changes and treatment with metformin both reduced the incidence of diabetes in persons at high risk. The lifestyle intervention was more effective than metformin. (N Engl J Med 2002; 346:393-403.)

Type II Diabetes

▪ stress and genetic components can lead to this ▪ it leads to damage of the blood vessels and heart disease ▪ 6 fold increase over last 40 years ▪ Is a disease of aging: Age 20-44: 3.7% Age 45-65: 13.7% Over 65: 26.9 ▪ Mechanism: - Excessive glucose in blood due to diet and obesity can lead to excessive insulin production and eventually insulin resistance

Fish Oil (Omega-3 Fatty Acids)

▪ they did a study on eskimos because they had really low rates of CVD ▪ their diet is mostly fish ▪ they found that eating fish once a week leads to a slight reduction of your risk of coronary heart disease

Twitter, Hostility, & CHD Mortality

▪ what's a methodological flaw? ▪ are the people who are tweeting the people who are dying of heart disease? --> probably not bc younger people tend to use twitter, but heart disease tends to happen more among older people *********************************************************** Eichstaedt et al Seligman 2015 Psychological language on Twitter predicts county-level Heart Disease Data - Psych Science Hostility and chronic stress are known risk factors for heart disease, but they are costly to assess on a large scale. We used language expressed on Twitter to characterize community-level psychological correlates of age-adjusted mortality from atherosclerotic heart disease (AHD). Language patterns reflecting negative social relationships, disengagement, and negative emotions—especially anger—emerged as risk factors; positive emotions and psychological engagement emerged as protective factors. Most correlations remained significant after controlling for income and education. A cross-sectional regression model based only on Twitter language predicted AHD mortality significantly better than did a model that combined 10 common demographic, socioeconomic, and health risk factors, including smoking, diabetes, hypertension, and obesity. Capturing community psychological characteristics through social media is feasible, and these characteristics are strong markers of cardiovascular mortality at the community level