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No data exist on the associations of dietary tomato and lycopene consumption with total and cause-specific mortality. Using the National Health and Nutrition Examination Surveys (NHANES) 1999-2010, we evaluted the long-term impact of tomato and lycopene intake on total and cause-specific (coronary heart disease [CHD] and cerebrovascular disease) mortality. We also assessed the changes in cardio-metabolic risk factors according to tomato and lycopene intake. Vital status through December 31, 2011 was ascertained. Cox proportional hazard regression models (followed by propensity score-matching) were used to investigate the link between tomato and lycopene consumption total, CHD and cerebrovascular mortality. Among the 23,935 participants included (mean age = 47.6 years, 48.8% men), 3403 deaths occurred during 76.4 months of follow-up. Tomato intake was inversely associated with total (risk ratio (RR):0.86, 95% confidence interval (CI):0.81-0.92), CHD (0.76, 95%CI: 0.70-0.85) and cerebrovascular (0.70, 95%CI: 0.62-0.81) mortality. Similar inverse associations were found between lycopene consumption, total (0.76, 95%CI: 0.72-0.81), CHD (0.73, 95%CI: 0.65-0.83) and cerebrovascular (0.71, 95%CI: 0.65-0.78) mortality; these associations were independent of anthropometric, clinical and nutritional parameters. Age and obesity did not affect the associations of tomato and lycopene consumption with total, CHD and cerebrovascular mortality. C-reactive protein significantly moderated the link between lycopene and tomato intake with total, CHD and cerebrovascular mortality. Analysis of co-variance showed that participants with a higher tomato and lycopene consumption had a more cardio-protective profile compared with those with a lower intake. Our results highlighted the favorable effect of tomato and lycopene intake on total and cause-specific mortality as well as to cardio-metabolic risk factors. These findings should be taken into consideration for public health strategies.
This study was performed to evaluate the effects of vitamin D and n-3 fatty acids’ co-supplementation on markers of cardiometabolic risk in diabetic patients with CHD. This randomised, double-blinded, placebo-controlled trial was conducted among sixty-one vitamin D-deficient diabetic patients with CHD. At baseline, the range of serum 25-hydroxyvitamin D levels in study participants was 6·3–19·9 ng/ml. Subjects were randomly assigned into two groups either taking 50 000 IU vitamin D supplements every 2 weeks plus 2× 1000 mg/d n-3 fatty acids from flaxseed oil (n 30) or placebo (n 31) for 6 months. Vitamin D and n-3 fatty acids’ co-supplementation significantly reduced mean (P = 0·01) and maximum levels of left carotid intima–media thickness (CIMT) (P = 0·004), and mean (P = 0·02) and maximum levels of right CIMT (P = 0·003) compared with the placebo. In addition, co-supplementation led to a significant reduction in fasting plasma glucose (β −0·40 mmol/l; 95 % CI −0·77, −0·03; P = 0·03), insulin (β −1·66 μIU/ml; 95 % CI −2·43, −0·89; P < 0·001), insulin resistance (β −0·49; 95 % CI −0·72, −0·25; P < 0·001) and LDL-cholesterol (β −0·21 mmol/l; 95 % CI −0·41, −0·01; P = 0·04), and a significant increase in insulin sensitivity (β +0·008; 95 % CI 0·004, 0·01; P = 0·001) and HDL-cholesterol (β +0·09 mmol/l; 95 % CI 0·01, 0·17; P = 0·02) compared with the placebo. Additionally, high-sensitivity C-reactive protein (β −1·56 mg/l; 95 % CI −2·65, −0·48; P = 0·005) was reduced in the supplemented group compared with the placebo group. Overall, vitamin D and n-3 fatty acids’ co-supplementation had beneficial effects on markers of cardiometabolic risk.
We aimed to develop, deliver and evaluate a brief training programme for primary care mental health staff in NW London focussing on long-term physical health conditions (LTCs). The objective was to improve participants’ knowledge, understanding and confidence (self-efficacy) in providing effective support to people with LTCs. The second objective was to develop an online version to be made available more widely.
The project was commissioned by NW London Collaboration of Clinical Commissioning Groups as part of a strategy to develop more joined up care and support for people with mental health needs. Training was developed by a team of experts, with input from commissioners, service users, clinicians and service managers.
Training was delivered via two-day interactive workshops providing: (i) key facts (informed by a review of published research and publically available health information); (ii) opportunity to engage with the ‘lived experience’ of people with LTCs (via videos, role plays, case studies and group discussion); (iii) skills-based training (in specific assessment and intervention methods). Knowledge, understanding and confidence (with respect to supporting people with LTCs) were assessed at the start and end of the training. An online training programme (with embedded evaluation questionnaire) was also developed, covering the same themes as the workshop.
Mental health staff (n=60) reported limited knowledge, understanding and confidence before the workshop, underlining the need for training. Knowledge of LTCs improved significantly following training (P<0.0001), along with awareness of the impact of poor psychological wellbeing on physical health (P<0.05) and the role of psychological therapies in supporting people with LTCs (P<0.0001). Self-efficacy also improved (P<0.001). Online training was accessed by 894 participants in the first six months and 187 provided feedback via the evaluation questionnaire. Responses indicated that participants found the training useful (88%), interesting (91%) and easy to understand (97%).
The theory, in brief outline here, implicating deficiency of Cu in the aetiology and pathophysiology of IHD explains more attributes of the disease than any other theory. This theory satisfies several of Hill’s criteria of a half-century ago for deducing association between an environmental feature and presence of an illness. Most important is the temporal association between the rise of IHD and the decrease in dietary Cu since the 1930s along with a parallel increase in the supplementation of pregnant women with Fe, a Cu antagonist. There are more than eighty anatomical, chemical and physiological similarities between animals deficient in Cu and individuals with IHD. Few of these similarities have been produced by other dietary manipulations because feeding cholesterol induces Cu deficiency in animals. The most recent of these to be identified is decreased serum dehydroepiandrosterone. Some concomitant aspects of Cu metabolism and utilisation have been identified in other theories about heart disease: fetal programming, homocysteine, and Fe overload.
Substantial healthcare resources are devoted to panic disorder (PD) and coronary heart disease (CHD); however, the association between these conditions remains controversial. Our objective was to conduct a systematic review of studies assessing the association between PD, related syndromes, and incident CHD.
Relevant studies were retrieved from Medline, EMBASE, SCOPUS and PsycINFO without restrictions from inception to January 2015 supplemented with hand-searching. We included studies that reported hazard ratios (HR) or sufficient data to calculate the risk ratio and 95% confidence interval (CI) which were pooled using a random-effects model. Studies utilizing self-reported CHD were ineligible. Twelve studies were included comprising 1 131 612 persons and 58 111 incident CHD cases.
PD was associated with the primary incident CHD endpoint [adjusted HR (aHR) 1.47, 95% CI 1.24–1.74, p < 0.00001] even after excluding angina (aHR 1.49, 95% CI 1.22–1.81, p < 0.00001). High to moderate quality evidence suggested an association with incident major adverse cardiac events (MACE; aHR 1.40, 95% CI 1.16–1.69, p = 0.0004) and myocardial infarction (aHR 1.36, 95% CI 1.12–1.66, p = 0.002). The risk for CHD was significant after excluding depression (aHR 1.64, 95% CI 1.45–1.85) and after depression adjustment (aHR 1.38, 95% CI 1.03–1.87). Age, sex, length of follow-up, socioeconomic status and diabetes were sources of heterogeneity in the primary endpoint.
Meta-analysis showed that PD was independently associated with incident CHD, myocardial infarction and MACE; however, reverse causality cannot be ruled out and there was evidence of heterogeneity.
This study assesses the feasibility of collecting genetic samples and self-reported outcome measures after cardiovascular risk assessment, and presenting the genetic test results to participants.
Coronary heart disease (CHD) genetic tests are increasingly available through direct-to-consumer marketing, but their potential clinical impact on cardiovascular risk assessment is unclear.
Observational study in 10 British general practices in Central England. A total of 320 individuals, who had completed conventional cardiovascular risk assessment, were offered CHD genetic test, with follow-up outcome questionnaire at eight months for lifestyle change and State-Trait Anxiety.
A total of 119 (37%) participants returned genetic test specimens, with over a third reporting family history of CHD in a specified relative; 79 (66.4%) were categorized above-average risk on conventional cardiovascular risk assessment, 65 of whom (82.3%) were only average risk on genetic assessment. The dietary fat questionnaire was poorly completed while study participation was not associated with increased anxiety (mean increase in anxiety score=2.1; 95% CI −0.1–4.3; P=0.06).
As a feasibility study, over a third of individuals offered genetic testing in primary care, as part of CVD risk assessment, took up the offer. Although intervention did not appear to increase anxiety, this needs further evaluation. To improve generalizability and effect size, future studies should actively engage individuals from wider socio-economic backgrounds who may not have already contemplated lifestyle change. The current research suggests general practitioners will face the clinical challenge of patients presenting with direct-to-consumer genetic results that are inconsistent with conventional cardiovascular risk assessment.
Some studies have found a significant relationship between birth weight (BW) and the risk of coronary heart disease (CHD) in adulthood, but results were inconsistent. The purpose of this study was to characterize the association between BW and the risk of CHD in adults. Among 144 papers detected by our search, 27 papers provided data on the relationship between BW and CHD, of which 23 papers considered BW as a continuous variable, and 14 articles considered BW as a categorical variable for this meta-analysis. Based on 23 papers, the mean weighted estimate for the association between BW and the combined outcome of non-fatal and fatal CHD was 0.83 [95% confidence interval (CI), 0.80–0.86] per kilogram of BW (P<0.0001). Low birth weight (LBW<2500 g) was associated with increased risk of CHD [odds ratio (OR), 1.19; 95% confidence interval (CI), 1.11–1.27] compared with subjects with BW⩾2500 g. LBW, as compared with normal BW (2500–4000 g), was associated with increased risk of CHD (OR, 1.16; 95% CI, 1.08–1.25). High birth weight (HBW⩾4000 g) was associated with decreased risk of CHD (OR, 0.89; 95% CI, 0.81–0.98) compared with subjects with BW<4000 g. In addition, there was an indication (not quite significant) that HBW was associated with a lower risk of CHD (OR, 0.89; 95% CI, 0.79–1.01), as compared with normal BW. No significant evidence of publication bias was present. These results suggest that LBW is significantly associated with increased risk of CHD and a 1 kg higher BW is associated with a 10–20% lower risk of CHD.
Antidepressants reduce depressive symptoms in patients with coronary heart disease, but they may be associated with increased mortality. This study aimed to examine whether the use of tricyclic antidepressants (TCA) or selective serotonin reuptake inhibitors (SSRI) is associated with mortality in patients with coronary heart disease, and to determine whether this association is mediated by autonomic function.
A total of 956 patients with coronary heart disease were followed for a mean duration of 7.2 years. Autonomic function was assessed as heart rate variability, and plasma and 24-h urinary norepinephrine.
Of 956 patients, 44 (4.6%) used TCA, 89 (9.3%) used SSRI, and 823 (86.1%) did not use antidepressants. At baseline, TCA users exhibited lower heart rate variability and higher norepinephrine levels compared with SSRI users and antidepressant non-users. At the end of the observational period, 52.3% of the TCA users had died compared with 38.2% in the SSRI group and 37.3% in the control group. The adjusted hazard ratio (HR) for TCA use compared with non-use was 1.74 [95% confidence interval (CI) 1.12–2.69, p = 0.01]. Further adjustment for measures of autonomic function reduced the association between TCA use and mortality (HR = 1.27, 95% CI 0.67–2.43, p = 0.47). SSRI use was not associated with mortality (HR = 1.15, 95% CI 0.81–1.64, p = 0.44).
The use of TCA was associated with increased mortality. This association was at least partially mediated by differences in autonomic function. Our findings suggest that TCA should be avoided in patients with coronary heart disease.
This study aimed to determine whether depression in patients with long-term conditions is associated with the number of morbidities or the type of co-morbidity.
A cohort study of 299 912 participants aged 30–100 years. The prevalence of depression, rates of health-care utilization and costs were evaluated in relation to diagnoses of diabetes mellitus (DM), coronary heart disease (CHD), stroke and colorectal cancer.
The age-standardized prevalence of depression was 7% in men and 14% in women with no morbidity. The frequency of depression increased in single morbidities including DM (men 13%, women 22%), CHD (men 15%, women 24%), stroke (men 14%, women 26%) or colorectal cancer (men 10%, women 21%). Participants with concurrent diabetes, CHD and stroke had a very high prevalence of depression (men 23%, women 49%). The relative rate of depression for one morbidity was 1.63 [95% confidence interval (CI) 1.59–1.66], two morbidities 1.96 (95% CI 1.89–2.03) and three morbidities 2.35 (95% CI 2.03–2.59). Compared to those with no morbidity, depression was associated with higher rates of health-care utilization and increased costs at any level of morbidity. In women aged 55 to 64 years without morbidity, the mean annual health-care cost was £513 without depression and £1074 with depression; when three morbidities were present, the cost was £1495 without depression and £2878 with depression.
Depression prevalence and health-care costs are more strongly associated with the number of morbidities than the nature of the co-morbid diagnosis.
Depression is common in chronic illness and screening for depression has been widely recommended. There have been no large studies of screening for depression in routine care for patients with chronic illness.
We performed a retrospective cohort study to examine the timing of new depression diagnosis or treatment in relation to annual screening for depression in patients with coronary heart disease (CHD) or diabetes. We examined a database derived from 1.3 million patients registered with general practices in Scotland for the year commencing 1 April 2007. Eligible patients had either CHD or diabetes, were screened for depression during the year and either received a new diagnosis of depression or commenced a new course of antidepressant (excluding those commonly used to treat diabetic neuropathy). Analysis was by the self-controlled case-series method with the outcome measure being the relative incidence (RI) in the period 1–28 days after screening compared to other times.
A total of 67358 patients were screened for depression and 2269 received a new diagnosis or commenced treatment. For the period after screening, the RI was 3.03 [95% confidence interval (CI) 2.44–3.78] for diagnosis and 1.78 (95% CI 1.54–2.05) for treatment. The number needed to screen was 976 (95% CI 886–1104) for a new diagnosis and 687 (95% CI 586–853) for new antidepressant treatment.
Systematic screening for depression in patients with chronic disease in primary care results in a significant but small increase in new diagnosis and treatment in the following 4 weeks.
Depressed mood following an acute coronary syndrome (ACS) is a risk factor for future cardiac morbidity. Hypothalamic–pituitary–adrenal (HPA) axis dysregulation is associated with depression, and may be a process through which depressive symptoms influence later cardiac health. Additionally, a history of depression predicts depressive symptoms in the weeks following ACS. The purpose of this study was to determine whether a history of depression and/or current depression are associated with the HPA axis dysregulation following ACS.
A total of 152 cardiac patients completed a structured diagnostic interview, a standardized depression questionnaire and a cortisol profile over the day, 3 weeks after an ACS. Cortisol was analysed using: the cortisol awakening response (CAR), total cortisol output estimated using the area under the curve method, and the slope of cortisol decline over the day.
Total cortisol output was positively associated with history of depression, after adjustment for age, gender, marital status, ethnicity, smoking status, body mass index (BMI), Global Registry of Acute Cardiac Events (GRACE) risk score, days in hospital, medication with statins and antiplatelet compounds, and current depression score. Men with clinically diagnosed depression after ACS showed a blunted CAR, but the CAR was not related to a history of depression.
Patients with a history of depression showed increased total cortisol output, but this is unlikely to be responsible for associations between depression after ACS and later cardiac morbidity. However, the blunted CAR in patients with severe depression following ACS indicates that HPA dysregulation is present.
In 1991, the Committee on Medical Aspects of Food Policy produced a report on the dietary reference values for food energy and nutrients for groups of people in the United Kingdom. The resulting recommendations, which included specific limits for intakes of total, saturated, trans- and cis-polyunsaturated fatty acids (PUFA) have remained a cornerstone of public health policy ever since, and similar recommendations have been adopted by the World Health Organization. These recommendations were made largely on the basis of specific effects of these fatty acids on the risk of developing atherosclerotic cardiovascular disease (CVD). The intervening years have seen a plethora of human epidemiological and intervention trials to further elucidate the specific relationship between dietary fatty acid intake, plasma lipids and lipoproteins and cardiovascular morbidity and mortality. A number of recent meta-analyses and systematic reviews have revisited the role of specific dietary fatty acid classes and CVD risk. In general, these continue to support a link between saturated fatty acids (SFA) and CVD morbidity/mortality. They also highlight the potent adverse effects of trans fatty acids derived from partially hydrogenated vegetable oil. The most recent data suggest that replacing SFA with cis-PUFA (primarily linoleic acid) has the greatest impact on reducing CVD risk. Evidence of specific beneficial effects of n-3 PUFA is generally stronger for secondary, rather than primary, CVD risk, and it is restricted to very long chain fatty acids of marine origin as opposed to alpha-linolenic acid. Taken together, these data suggest that recent focus on dietary n-6-to-n-3 PUFA ratios may have been misguided, and that future strategies should focus on replacing dietary SFA with total PUFA, rather than concentrating on n-6 : n-3 PUFA ratio.
This paper was originally written for a conference entitled ‘The Future of Medical History. Now it ought to be clear – certainly to historians – that the future of anything is hard to predict; but at least in the short term, any future for medical history seems likely to include the history of disease, and the history of coronary heart disease (CHD) provides an excellent example of what the history of disease has to offer to a wide range of audiences.
Depression following myocardial infarction (MI) independently increases risk for early cardiac morbidity and mortality. Studies suggest that somatic, but not cognitive, depressive symptoms are responsible for the increased risk. However, the effects of somatic depressive symptoms at follow-up, after sufficient time has elapsed to allow for physical recovery from the initial infarction, are not known. Our aim was to examine the relationship between cognitive and somatic depressive symptom dimensions at baseline and 12 months post-MI and subsequent mortality and cardiovascular morbidity.
Patients were 2442 depressed and/or socially isolated men and women with acute MI included in the Enhancing Recovery in Coronary Heart Disease (ENRICHD) clinical trial. We used principal components analysis (PCA) of the Beck Depression Inventory (BDI) items to derive subscales measuring cognitive and somatic depressive symptom dimensions, and Cox regression with Bonferroni correction for multiple testing to examine the contribution of these dimensions to all-cause mortality, cardiovascular mortality, and first recurrent non-fatal MI.
After adjusting for medical co-morbidity and Bonferroni correction, the somatic depressive symptom dimension assessed proximately following MI did not significantly predict any endpoints. At 12 months post-MI, however, this dimension independently predicted subsequent all-cause [hazard ratio (HR) 1.43, 95% confidence interval (CI) 1.13–1.81] and cardiovascular mortality (HR 1.60, 95% CI 1.17–2.18). No significant associations were found between the cognitive depressive symptom dimension and any endpoints after Bonferroni correction.
Somatic symptoms of depression at 12 months post-MI in patients at increased psychosocial risk predicted subsequent mortality. Psychosocial interventions aimed at improving cardiac prognosis may be enhanced by targeting somatic depressive symptoms, with particular attention to somatic symptom severity at 12 months post-MI.
The objective of the present study was to determine whether the consumption of ≥ 250 v. < 250 mg of the long-chain n-3 fatty acids (n-3 LCFA) per d is associated with a reduction in the risk of fatal and non-fatal CHD in individuals with no prior history of CHD. A comprehensive and systematic review of the published scientific literature resulted in the identification of eight prospective studies (seven cohorts and one nested case–control study) that met predefined inclusion criteria. Relative to the consumption of < 250 mg n-3 LCFA per d, the consumption of ≥ 250 mg/d was associated with a significant 35·1 % reduction in the risk of sudden cardiac death and a near-significant 16·6 % reduction in the risk of total fatal coronary events, while the risk of non-fatal myocardial infarction was not significantly reduced. In several meta-analyses, which were based on US studies, risk of CHD death was found to be dose-dependently reduced by the n-3 LCFA, with further risk reductions observed with intakes in excess of 250 mg/d. Prospective observational and intervention data from Japan, where intake of fish is very high, suggest that n-3 LCFA intakes of 900 to 1000 mg/d and greater may confer protection against non-fatal myocardial infarction. Thus, the intake of 250 mg n-3 LCFA per d may, indeed, be a minimum target to be achieved by the general population for the promotion of cardiovascular health.
Objectives: The Secondary Prevention of Heart disEase in geneRal practicE (SPHERE) trial has recently reported. This study examines the cost-effectiveness of the SPHERE intervention in both healthcare systems on the island of Ireland.
Methods: Incremental cost-effectiveness analysis. A probabilistic model was developed to combine within-trial and beyond-trial impacts of treatment to estimate the lifetime costs and benefits of two secondary prevention strategies: Intervention - tailored practice and patient care plans; and Control - standardized usual care.
Results: The intervention strategy resulted in mean cost savings per patient of €512.77 (95 percent confidence interval [CI], −1086.46–91.98) and an increase in mean quality-adjusted life-years (QALYs) per patient of 0.0051 (95 percent CI, −0.0101–0.0200), when compared with the control strategy. The probability of the intervention being cost-effective was 94 percent if decision makers are willing to pay €45,000 per additional QALY.
Conclusions: Decision makers in both settings must determine whether the level of evidence presented is sufficient to justify the adoption of the SPHERE intervention in clinical practice.
Although a substantial body of research points to a link between psychological distress and inflammatory responses in middle-aged and older adults, particularly those with cardiovascular disease, the relationship between inflammation and distress in young, healthy individuals has not been established. This study was designed to investigate the cross-sectional association between psychological distress and inflammatory proteins in a young, healthy representative population of English adults.
Participants were 1338 individuals aged 16–34 years from the 2006 Health Survey for England (HSE). Blood samples to measure plasma fibrinogen and high sensitivity C-reactive protein (hsCRP), as well as measures of psychological distress (using the General Health Questionnaire 12-item scale, GHQ-12) and covariates, were collected during home visits. Linear regression was used to assess the relationship between psychological distress and fibrinogen and hsCRP.
Higher self-rated distress was positively associated with fibrinogen level in this young population, independently of age, sex, ethnicity, body mass index (BMI), high density lipoprotein (HDL) cholesterol, smoking, and alcohol and medication use (β=0.024, p<0.01). Psychological distress was not related to hsCRP.
Psychological distress may negatively impact inflammatory processes in young adulthood before the onset of chronic health problems such as hypertension and cardiovascular disease. Longitudinal research is needed to elucidate the relationship between distress and inflammation in young adults and its significance for later disease states.
To examine the prevalence and likelihood of taking folic acid or vitamin supplements among adults with CHD or stroke v. adults without these conditions.
A cross-sectional Behavioural Risk Factor Surveillance System survey was conducted in twelve states of the United States and Puerto Rico in 2006. Self-reported data from participants were collected.
The United States.
US non-institutionalised adults (n 41 792), aged ≥45 years.
Of all participants, 5445 had CHD and 2076 had stroke. Significantly higher percentages of women than men reported taking folic acid or vitamin supplements. After adjustment for potential confounders, women with CHD had a significantly lower adjusted prevalence (AP) and adjusted OR (AOR) than women without CHD for taking folic acid less than one time per d (AP = 3·9 % v. 5·5 %; AOR = 0·56; 95 % CI 0·39, 0·81), for taking folic acid one to four times per d (AP = 50·0 % v. 57·5 %; AOR = 0·68; 95 % CI 0·60, 0·79), and for taking vitamin supplements (AP = 60·9 % v. 69·9 %; AOR = 0·66; 95 % CI 0·57, 0·76). Men with CHD had a significantly higher AP (50·4 % v. 46·2 %) and AOR (1·17; 95 % CI 1·02, 1·33) of taking folic acid one to four times per d than men without CHD. In both sexes, adults with stroke were as likely as those without to take these supplements.
Substantial variations in the prevalence and likelihood of taking folic acid or vitamin supplements exist by gender and by CHD status, but not by stroke status.
We evaluated the effects of peanut consumption on lipid profiles, atherogenic index of plasma (AIP) and CHD risk in hypercholesterolaemic men.
Randomised crossover clinical trial.
Participants were randomly assigned to two groups. They were asked to consume peanut supplements (about 77 g) with their habitual diet for 4 weeks.
Fifty-four hypercholesterolaemic men with total cholesterol (TC) concentrations between 200 and 350 mg/dl.
Compared with the habitual diet, peanut supplementation of the habitual diet significantly reduced TC/HDL cholesterol (HDL-C) ratio (mean 1 (se 0·3) P = 0·001) and LDL cholesterol (LDL-C)/HDL-C ratio (mean 0·7 (se 0·2); P = 0·001). Peanut consumption increased HDL-C (mean 6·1 (se 1·5) mg/dl; P < 0·001) and total antioxidant capacity (TAC) (mean 1·2 (se 0·6) U/mL P = 0·04). In addition, peanut consumption significantly reduced the AIP (mean 0·1 (se 0·03) P = 0·01) and CHD estimated risk over 10 years based on systolic and diastolic blood pressures (mean 1·4 % (se 0·5 %) P = 0·004 and mean 2·2 % (se 0·5 %) P < 0·001, respectively).
Short-term peanut consumption might improve lipid profiles, the AIP and CHD risk in free-living hypercholesterolaemic men.
Regular physical activity and exercise result in positive improvements in health and fitness. Moderate amounts of physical activity can reduce the risk of certain types of cancer, heart disease, diabetes, and obesity. Burning approximately 150 kilocalories per day or 1,000 kilocalories per week leads to a reduction in the risk of coronary heart disease by 50% and of hypertension, diabetes, and colon cancer by 30%. The evidence for exercise providing a reduction in the risk of breast cancer is equivocal. Women who are physically active have higher resting metabolic rates and lower body fat, but similar fat-free mass, body mass index, and body weight compared to their sedentary counterparts. The type of exercise performed depends on the desired goal. If a woman wants to build muscular strength, then resistance training is appropriate. Exercise prescriptions for a female athlete are specific to the demands of her sport.