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Effect of a multi-domain lifestyle intervention on cardiovascular risk in older people: the FINGER trial.
Lehtisalo, J, Rusanen, M, Solomon, A, Antikainen, R, Laatikainen, T, Peltonen, M, Strandberg, T, Tuomilehto, J, Soininen, H, Kivipelto, M, et al
European heart journal. 2022;43(21):2054-2061
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Older people are at high risk of cardiovascular disease, and 90% of the risk factors can be modified, including an unhealthy diet, poor physical activity, obesity, smoking, and obesity-related comorbidities. This randomised controlled trial examined a multifactorial approach combining several lifestyle modifications in 1259 older adults between 60 and 77 years of age to reduce the risk of cardiovascular disease. Participants were randomly assigned to intensive multi-domain lifestyle intervention or regular health advice control groups. The multifactorial lifestyle intervention incorporated dietary counselling, exercise training, cognitive training, and managing CVD and metabolic risk factors. Dietary interventions included tailored strategies that considered increased consumption of fruits, berries, vegetables, whole grains, margarine, oil, and fish. Physical exercise interventions included strength training, balance exercises, and aerobic exercises. Cognitive interventions and intensive strategies to manage metabolic factors were also implemented. In the multifactorial lifestyle intervention group, cerebrovascular events were lower after two years than in the control group. In addition, cardiovascular disease and stroke incidence were lower in the elderly with a history of cardiovascular disease. Healthcare professionals can use the results from this study to understand the benefits of multifactorial lifestyle interventions on cardiovascular disease. However, there is a need for longer-term robust studies since the evidence is sparse.
Abstract
AIMS: Joint prevention of cardiovascular disease (CVD) and dementia could reduce the burden of both conditions. The Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) demonstrated a beneficial effect on cognition (primary outcome) and we assessed the effect of this lifestyle intervention on incident CVD (pre-specified secondary outcome). METHODS AND RESULTS FINGER enrolled 1259 individuals aged 60-77 years (ClinicalTrials.gov NCT01041989). They were randomized (1:1) to a 2-year multi-domain intervention with diet, physical and cognitive activity, and vascular monitoring (n = 631), or general health advice (n = 628). National registries provided data on CVD including stroke, transient ischaemic attack (TIA), or coronary heart event. During an average of 7.4 years, 229 participants (18%) had at least one CVD diagnosis: 107 in the intervention group and 122 in the control group. The incidence of cerebrovascular events was lower in the intervention than the control group: hazard ratio (HR) for combined stroke/TIA was 0.71 [95% confidence interval (CI): 0.51-0.99] after adjusting for background characteristics. Hazard ratio for coronary events was 0.84 (CI: 0.56-1.26) and total CVD events 0.80 (95% CI: 0.61-1.04). Among those with history of CVD (n = 145), the incidence of both total CVD events (HR: 0.50, 95% CI: 0.28-0.90) and stroke/TIA (HR: 0.40, 95% CI: 0.20-0.81) was lower in the intervention than the control group. CONCLUSION A 2-year multi-domain lifestyle intervention among older adults was effective in preventing cerebrovascular events and also total CVD events among those who had history of CVD.
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Linoleic Acid-Rich Oil Alters Circulating Cardiolipin Species and Fatty Acid Composition in Adults: A Randomized Controlled Trial.
Cole, RM, Angelotti, A, Sparagna, GC, Ni, A, Belury, MA
Molecular nutrition & food research. 2022;66(15):e2101132
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Dietary polyunsaturated fatty acid intake is associated with reduced cardiometabolic disease risk. In addition, higher linoleic acid (LA) biomarkers have been associated with a reduced risk for cardiometabolic diseases and conditions. The main aim of this study was to determine whether a modest addition of an oil rich in LA could change the LA content in plasma, erythrocytes, and peripheral blood mononuclear cells (PBMCs). The secondary aim was to determine if the LA-rich oil could alter cardiolipin species in PBMCs. This study is a randomised double-masked placebo-controlled study of 84 participants who were randomly assigned to one of the two groups: either the high-oleate-cookie (n = 42) or LA-cookie groups (n = 42). Results show that dietary supplementation with less than one serving of LA-rich oil per day increases LA in PBMC cardiolipin as well as LA levels. Authors conclude that patients with obesity, cardiometabolic disease, and other conditions related to mitochondrial dysfunction could be a future cohort that should be studied.
Abstract
SCOPE Higher circulating linoleic acid (LA) and muscle-derived tetralinoleoyl-cardiolipin (LA4 CL) are each associated with decreased cardiometabolic disease risk. Mitochondrial dysfunction occurs with low LA4 CL. Whether LA-rich oil fortification can increase LA4 CL in humans is unknown. The aims of this study are to determine whether dietary fortification with LA-rich oil for 2 weeks increases: 1) LA in plasma, erythrocytes, and peripheral blood mononuclear cells (PBMC); and 2) LA4 CL in PBMC in adults. METHODS AND RESULTS In this randomized controlled trial, adults are instructed to consume one cookie per day delivering 10 g grapeseed (LA-cookie, N = 42) or high oleate (OA) safflower (OA-cookie, N = 42) oil. In the LA-cookie group, LA increases in plasma, erythrocyte, and PBMC by 6%, 7%, and 10% respectively. PBMC and erythrocyte OA increase by 7% and 4% in the OA-cookie group but is unchanged in the plasma. PBMC LA4 CL increases (5%) while LA3 OA1 CL decreases (7%) in the LA-cookie group but are unaltered in the OA-cookie group. CONCLUSIONS LA-rich oil fortification increases while OA-oil has no effect on LA4 CL in adults. Because LA-rich oil fortification reduces cardiometabolic disease risk and increases LA4 CL, determining whether mitochondrial dysfunction is repaired through dietary fortification is warranted.
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A Systematic Review of the Association Between Vegan Diets and Risk of Cardiovascular Disease.
Kaiser, J, van Daalen, KR, Thayyil, A, Cocco, MTARR, Caputo, D, Oliver-Williams, C
The Journal of nutrition. 2021;151(6):1539-1552
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Plant-based diets have increased in popularity due to concerns for the environment and animal welfare and due to perceived health benefits. The aim of this study was to assess the association between vegan diets and risks of primary, intermediate, and recurrent cardiovascular disease (CVD). This study is a systemic review of 7 epidemiological studies comprising over 73,000 participants, of whom at least 7661 were vegans. Results indicate that there was no significant evidence of an association between adherence to a vegan diet and risks of primary CVD or a coronary heart disease event. Authors conclude that further experimental evidence and research in large diverse cohorts is required in order to better understand the clinical relevance and public health implications of the vegan diet.
Abstract
BACKGROUND Plant-based diets are gaining attention globally due to their environmental benefits and perceived health-protective role. A vegan diet may have cardiovascular benefits; however, evidence remains conflicting and insufficiently assessed. OBJECTIVES We evaluated the utility of the vegan diet in cardiovascular disease (CVD) prevention. METHODS We conducted a systematic review of studies evaluating the association between vegan diets and cardiovascular outcomes. We searched 5 databases (Ovid MEDLINE, EMBASE, Web of Science, Scopus, and OpenGrey) through 31 October 2020. Four investigators independently screened the full texts for inclusion, assessed quality, and extracted data from published reports. RESULTS Out of the 5729 identified records, 7 were included, comprising over 73,000 participants, of whom at least 7661 were vegans. Three studies, with at least 73,426 individuals (including at least 7380 vegans), examined risks of primary cardiovascular events (total CVD, coronary heart disease, acute myocardial infarction, total stroke, hemorrhagic stroke, and ischemic stroke) in individuals who followed a vegan diet compared to those who did not. None of the studies reported a significantly increased or decreased risk of any cardiovascular outcome. One study suggested that vegans were at greater risk of ischemic stroke compared to individuals who consumed animal products (HR, 1.54; 95% CI, 0.95-2.48). Yet in another study, vegans showed lower common carotid artery intima-media thickness (0.56 ± 0.1 mm vs. 0.74 ± 0.1 mm in controls; P < 0.001), and in 3 studies of recurrent CVD events, vegans had 0-52% lower rates. Furthermore, endothelial function did not differ between vegans and nonvegans. Using the Grading of Recommendations Assessment, Development and Evaluation approach, evidence was deemed to be of low to very low strength/quality. CONCLUSIONS Among the Western populations studied, evidence weakly demonstrates associations between vegan diets and risk of CVDs, with the direction of associations varying with the specific CVD outcome tested. However, more high-quality research on this topic is needed. This study was registered at PROSPERO as CRD42019146835.
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Effect of Omega-3 Dosage on Cardiovascular Outcomes: An Updated Meta-Analysis and Meta-Regression of Interventional Trials.
Bernasconi, AA, Wiest, MM, Lavie, CJ, Milani, RV, Laukkanen, JA
Mayo Clinic proceedings. 2021;96(2):304-313
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There is mixed evidence to support the use of omega-3 fatty acids for the prevention and treatment of cardiovascular disease. Animal studies have shown promising results, but randomised control trials are inconsistent, possibly due to differing doses used, or differences in the subject’s omega-3 levels at the start of the trial. This meta-analysis of 40 studies with over 135,000 subjects aimed to determine whether omega-3 supplementation reduces heart disease risk and whether dosage has a role. The results showed that omega-3 supplementation reduced the risk of heart attacks, death from heart attacks and deaths due to heart disease, and the higher the dose, the greater the protection. The majority of studies were on individuals who had already had a heart attack or who had suffered from a related condition. It was concluded that supplementation with omega-3 is effective in preventing heart disease and heart attacks and the protective effect increases with dosage. This study could be used by healthcare professionals to prevent further heart disease and heart attacks in individuals who have already suffered from one of these conditions.
Abstract
OBJECTIVES To quantify the effect of eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids on cardiovascular disease (CVD) prevention and the effect of dosage. METHODS This study is designed as a random effects meta-analysis and meta-regression of randomized control trials with EPA/DHA supplementation. This is an update and expanded analysis of a previously published meta-analysis which covers all randomized control trials with EPA/DHA interventions and cardiovascular outcomes published before August 2019. The outcomes included are myocardial infarction (MI), coronary heart disease (CHD) events, CVD events (a composite of MI, angina, stroke, heart failure, peripheral arterial disease, sudden death, and non-scheduled cardiovascular surgical interventions), CHD mortality and fatal MI. The strength of evidence was assessed using the Grading of Recommendations Assessment, Development, and Evaluation framework. RESULTS A total of 40 studies with a combined 135,267 participants were included. Supplementation was associated with reduced risk of MI (relative risk [RR], 0.87; 95% CI, 0.80 to 0.96), high certainty number needed to treat (NNT) of 272; CHD events (RR, 0.90; 95% CI, 0.84 to 0.97), high certainty NNT of 192; fatal MI (RR, 0.65; 95% CI, 0.46 to 0.91]), moderate certainty NNT = 128; and CHD mortality (RR, 0.91; 95% CI, 0.85 to 0.98), low certainty NNT = 431, but not CVD events (RR, 0.95; 95% CI, 0.90 to 1.00). The effect is dose dependent for CVD events and MI. CONCLUSION Cardiovascular disease remains the leading cause of death worldwide. Supplementation with EPA and DHA is an effective lifestyle strategy for CVD prevention, and the protective effect probably increases with dosage.
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Coenzyme Q10 for heart failure.
Al Saadi, T, Assaf, Y, Farwati, M, Turkmani, K, Al-Mouakeh, A, Shebli, B, Khoja, M, Essali, A, Madmani, ME
The Cochrane database of systematic reviews. 2021;(2):CD008684
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As per the definition given by the NHS, heart failure happens when the heart fails to pump blood around the body due to stiffness or weakness of the heart muscle. Coenzyme Q10 reduces oxidative stress and toxic effects in the body by acting as a fat-soluble antioxidant nutrient. Due to these beneficial effects, CoQ10 may effectively reduce damage to cardiac cells and disruption to cellular signalling. CoQ10 is also a cell membrane stabiliser, and previous studies have shown a correlation between the severity of heart failure and CoQ10 deficiency. In addition, dietary absorption of CoQ10 is relatively slow and ineffective; therefore, supplementation is effective and safe with no side effects. This review included eleven randomised controlled studies to compare the beneficial effects of Coenzyme Q10 for the treatment of people with heart disease. This review showed that Coenzyme Q10 might reduce all-cause mortality and hospitalisation due to heart failure. In addition, CoQ10 may stabilise myocardial calcium‐dependent ion channels and encourage adenosine‐5'‐triphosphate (ATP) synthesis. However, the effectiveness of CoQ10 in lowering the risk of myocardial infarction or stroke, left ventricular ejection fraction and exercise capacity is inconclusive. Healthcare professionals can use this study's results to understand the potential beneficial effects of CoQ10 supplementation on maintaining heart health. However, due to the high heterogeneity in the current research, further robust long-term studies are required to evaluate the therapeutic value of Coenzyme Q10 in managing heart disease.
Abstract
BACKGROUND Coenzyme Q10, or ubiquinone, is a non-prescription nutritional supplement. It is a fat-soluble molecule that acts as an electron carrier in mitochondria, and as a coenzyme for mitochondrial enzymes. Coenzyme Q10 deficiency may be associated with a multitude of diseases, including heart failure. The severity of heart failure correlates with the severity of coenzyme Q10 deficiency. Emerging data suggest that the harmful effects of reactive oxygen species are increased in people with heart failure, and coenzyme Q10 may help to reduce these toxic effects because of its antioxidant activity. Coenzyme Q10 may also have a role in stabilising myocardial calcium-dependent ion channels, and in preventing the consumption of metabolites essential for adenosine-5'-triphosphate (ATP) synthesis. Coenzyme Q10, although not a primary recommended treatment, could be beneficial to people with heart failure. Several randomised controlled trials have compared coenzyme Q10 to other therapeutic modalities, but no systematic review of existing randomised trials was conducted prior to the original version of this Cochrane Review, in 2014. OBJECTIVES To review the safety and efficacy of coenzyme Q10 in heart failure. SEARCH METHODS We searched CENTRAL, MEDLINE, Embase, Web of Science, CINAHL Plus, and AMED on 16 October 2020; ClinicalTrials.gov on 16 July 2020, and the ISRCTN Registry on 11 November 2019. We applied no language restrictions. SELECTION CRITERIA We included randomised controlled trials of either parallel or cross-over design that assessed the beneficial and harmful effects of coenzyme Q10 in people with heart failure. When we identified cross-over studies, we considered data only from the first phase. DATA COLLECTION AND ANALYSIS We used standard Cochrane methods, assessed study risk of bias using the Cochrane 'Risk of bias' tool, and GRADE methods to assess the quality of the evidence. For dichotomous data, we calculated the risk ratio (RR); for continuous data, the mean difference (MD), both with 95% confidence intervals (CI). Where appropriate data were available, we conducted meta-analysis. When meta-analysis was not possible, we wrote a narrative synthesis. We provided a PRISMA flow chart to show the flow of study selection. MAIN RESULTS We included eleven studies, with 1573 participants, comparing coenzyme Q10 to placebo or conventional therapy (control). In the majority of the studies, sample size was relatively small. There were important differences among studies in daily coenzyme Q10 dose, follow-up period, and the measures of treatment effect. All studies had unclear, or high risk of bias, or both, in one or more bias domains. We were only able to conduct meta-analysis for some of the outcomes. None of the included trials considered quality of life, measured on a validated scale, exercise variables (exercise haemodynamics), or cost-effectiveness. Coenzyme Q10 probably reduces the risk of all-cause mortality more than control (RR 0.58, 95% CI 0.35 to 0.95; 1 study, 420 participants; number needed to treat for an additional beneficial outcome (NNTB) 13.3; moderate-quality evidence). There was low-quality evidence of inconclusive results between the coenzyme Q10 and control groups for the risk of myocardial infarction (RR 1.62, 95% CI 0.27 to 9.59; 1 study, 420 participants), and stroke (RR 0.18, 95% CI 0.02 to 1.48; 1 study, 420 participants). Coenzyme Q10 probably reduces hospitalisation related to heart failure (RR 0.62, 95% CI 0.49 to 0.78; 2 studies, 1061 participants; NNTB 9.7; moderate-quality evidence). Very low-quality evidence suggests that coenzyme Q10 may improve the left ventricular ejection fraction (MD 1.77, 95% CI 0.09 to 3.44; 7 studies, 650 participants), but the results are inconclusive for exercise capacity (MD 48.23, 95% CI -24.75 to 121.20; 3 studies, 91 participants); and the risk of developing adverse events (RR 0.70, 95% CI 0.45 to 1.10; 2 studies, 568 participants). We downgraded the quality of the evidence mainly due to high risk of bias and imprecision. AUTHORS' CONCLUSIONS The included studies provide moderate-quality evidence that coenzyme Q10 probably reduces all-cause mortality and hospitalisation for heart failure. There is low-quality evidence of inconclusive results as to whether coenzyme Q10 has an effect on the risk of myocardial infarction, or stroke. Because of very low-quality evidence, it is very uncertain whether coenzyme Q10 has an effect on either left ventricular ejection fraction or exercise capacity. There is low-quality evidence that coenzyme Q10 may increase the risk of adverse effects, or have little to no difference. There is currently no convincing evidence to support or refute the use of coenzyme Q10 for heart failure. Future trials are needed to confirm our findings.
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6-month neurological and psychiatric outcomes in 236 379 survivors of COVID-19: a retrospective cohort study using electronic health records.
Taquet, M, Geddes, JR, Husain, M, Luciano, S, Harrison, PJ
The lancet. Psychiatry. 2021;8(5):416-427
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Recent literature shows that COVID-19 survivors might be at an increased risk of neurological and psychiatric disorders. The aim of this study was to investigate the incidence of neurological and psychiatric diagnoses in survivors in the 6 months after documented clinical COVID-19 infection. This study is a retrospective cohort study with the primary cohort comprised of 236,379 patients diagnosed with COVID-19 and two propensity-score-matched control cohorts. The primary cohort was divided into one of the four subgroups. Results indicate that the severity of COVID-19 had a clear effect on subsequent neurological diagnoses. In fact, COVID-19 was associated with an increased risk of neurological and psychiatric outcomes. However, the incidences and hazard ratio of these were greater in patients who had required hospitalisation, and particularly those who required ITU admission or developed encephalopathy, even after extensive propensity score matching for other factors. Authors conclude that COVID-19 is followed by significant rates of neurological and psychiatric diagnoses over the subsequent 6 months.
Abstract
BACKGROUND Neurological and psychiatric sequelae of COVID-19 have been reported, but more data are needed to adequately assess the effects of COVID-19 on brain health. We aimed to provide robust estimates of incidence rates and relative risks of neurological and psychiatric diagnoses in patients in the 6 months following a COVID-19 diagnosis. METHODS For this retrospective cohort study and time-to-event analysis, we used data obtained from the TriNetX electronic health records network (with over 81 million patients). Our primary cohort comprised patients who had a COVID-19 diagnosis; one matched control cohort included patients diagnosed with influenza, and the other matched control cohort included patients diagnosed with any respiratory tract infection including influenza in the same period. Patients with a diagnosis of COVID-19 or a positive test for SARS-CoV-2 were excluded from the control cohorts. All cohorts included patients older than 10 years who had an index event on or after Jan 20, 2020, and who were still alive on Dec 13, 2020. We estimated the incidence of 14 neurological and psychiatric outcomes in the 6 months after a confirmed diagnosis of COVID-19: intracranial haemorrhage; ischaemic stroke; parkinsonism; Guillain-Barré syndrome; nerve, nerve root, and plexus disorders; myoneural junction and muscle disease; encephalitis; dementia; psychotic, mood, and anxiety disorders (grouped and separately); substance use disorder; and insomnia. Using a Cox model, we compared incidences with those in propensity score-matched cohorts of patients with influenza or other respiratory tract infections. We investigated how these estimates were affected by COVID-19 severity, as proxied by hospitalisation, intensive therapy unit (ITU) admission, and encephalopathy (delirium and related disorders). We assessed the robustness of the differences in outcomes between cohorts by repeating the analysis in different scenarios. To provide benchmarking for the incidence and risk of neurological and psychiatric sequelae, we compared our primary cohort with four cohorts of patients diagnosed in the same period with additional index events: skin infection, urolithiasis, fracture of a large bone, and pulmonary embolism. FINDINGS Among 236 379 patients diagnosed with COVID-19, the estimated incidence of a neurological or psychiatric diagnosis in the following 6 months was 33·62% (95% CI 33·17-34·07), with 12·84% (12·36-13·33) receiving their first such diagnosis. For patients who had been admitted to an ITU, the estimated incidence of a diagnosis was 46·42% (44·78-48·09) and for a first diagnosis was 25·79% (23·50-28·25). Regarding individual diagnoses of the study outcomes, the whole COVID-19 cohort had estimated incidences of 0·56% (0·50-0·63) for intracranial haemorrhage, 2·10% (1·97-2·23) for ischaemic stroke, 0·11% (0·08-0·14) for parkinsonism, 0·67% (0·59-0·75) for dementia, 17·39% (17·04-17·74) for anxiety disorder, and 1·40% (1·30-1·51) for psychotic disorder, among others. In the group with ITU admission, estimated incidences were 2·66% (2·24-3·16) for intracranial haemorrhage, 6·92% (6·17-7·76) for ischaemic stroke, 0·26% (0·15-0·45) for parkinsonism, 1·74% (1·31-2·30) for dementia, 19·15% (17·90-20·48) for anxiety disorder, and 2·77% (2·31-3·33) for psychotic disorder. Most diagnostic categories were more common in patients who had COVID-19 than in those who had influenza (hazard ratio [HR] 1·44, 95% CI 1·40-1·47, for any diagnosis; 1·78, 1·68-1·89, for any first diagnosis) and those who had other respiratory tract infections (1·16, 1·14-1·17, for any diagnosis; 1·32, 1·27-1·36, for any first diagnosis). As with incidences, HRs were higher in patients who had more severe COVID-19 (eg, those admitted to ITU compared with those who were not: 1·58, 1·50-1·67, for any diagnosis; 2·87, 2·45-3·35, for any first diagnosis). Results were robust to various sensitivity analyses and benchmarking against the four additional index health events. INTERPRETATION Our study provides evidence for substantial neurological and psychiatric morbidity in the 6 months after COVID-19 infection. Risks were greatest in, but not limited to, patients who had severe COVID-19. This information could help in service planning and identification of research priorities. Complementary study designs, including prospective cohorts, are needed to corroborate and explain these findings. FUNDING National Institute for Health Research (NIHR) Oxford Health Biomedical Research Centre.
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The COVID-19 Pandemic: a Call to Action to Identify and Address Racial and Ethnic Disparities.
Laurencin, CT, McClinton, A
Journal of racial and ethnic health disparities. 2020;7(3):398-402
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The severe acute respiratory syndrome coronavirus 2 virus was first identified in late 2019 in Wuhan, China. Various unsubstantiated reports emerged declaring that the genetic constitution of Blacks or even the presence of melanin rendered Blacks immune to the virus. This study is a call of action which reviews preliminary data on race and ethnicity in the peer-reviewed literature for citizens in America affected by COVID-19. Findings demonstrate that communities of colour (Blacks) have a higher rate of infection and death in comparison to their population percentage in the state of Connecticut. However, authors are unable to draw conclusions since race and ethnicity data is missing and the data in this paper is the earliest data available. Therefore, the authors call for action to identify and address racial and ethnic health disparities in the COVID-19 crisis.
Abstract
The Coronavirus disease 2019 (COVID-19) pandemic has significantly impacted and devastated the world. As the infection spreads, the projected mortality and economic devastation are unprecedented. In particular, racial and ethnic minorities may be at a particular disadvantage as many already assume the status of a marginalized group. Black Americans have a long-standing history of disadvantage and are in a vulnerable position to experience the impact of this crisis and the myth of Black immunity to COVID-19 is detrimental to promoting and maintaining preventative measures. We are the first to present the earliest available data in the peer-reviewed literature on the racial and ethnic distribution of COVID-19-confirmed cases and fatalities in the state of Connecticut. We also seek to explode the myth of Black immunity to the virus. Finally, we call for a National Commission on COVID-19 Racial and Ethnic Health Disparities to further explore and respond to the unique challenges that the crisis presents for Black and Brown communities.
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Egg consumption and risk of cardiovascular disease: three large prospective US cohort studies, systematic review, and updated meta-analysis.
Drouin-Chartier, JP, Chen, S, Li, Y, Schwab, AL, Stampfer, MJ, Sacks, FM, Rosner, B, Willett, WC, Hu, FB, Bhupathiraju, SN
BMJ (Clinical research ed.). 2020;368:m513
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Eggs have a high cholesterol content and have therefore been associated with a risk for heart disease. However, studies to substantiate this have been conflicting, with some studies showing associations and others not. This systematic review and meta-analysis of over five million people and 763 studies aimed to evaluate the association between egg intake and the risk of heart disease. The results showed that higher egg intake was associated with a poor diet. Egg intake was not associated with heart disease and this was evident even in people who ate at least one egg per day. Even in people with other associated diseases, such as type 2 diabetes and high blood pressure, egg intake was not associated with heart disease. It was concluded that egg consumption does not increase an individual’s risk for heart disease. This study could be used by healthcare professionals to justify the recommendation that patients at risk of heart disease or those who have heart disease, can still eat up to one egg per day, without risk of exacerbating their condition.
Abstract
OBJECTIVE To evaluate the association between egg intake and cardiovascular disease risk among women and men in the United States, and to conduct a meta-analysis of prospective cohort studies. DESIGN Prospective cohort study, and a systematic review and meta-analysis of prospective cohort studies. SETTING Nurses' Health Study (NHS, 1980-2012), NHS II (1991-2013), Health Professionals' Follow-Up Study (HPFS, 1986-2012). PARTICIPANTS Cohort analyses included 83 349 women from NHS, 90 214 women from NHS II, and 42 055 men from HPFS who were free of cardiovascular disease, type 2 diabetes, and cancer at baseline. MAIN OUTCOME MEASURES Incident cardiovascular disease, which included non-fatal myocardial infarction, fatal coronary heart disease, and stroke. RESULTS Over up to 32 years of follow-up (>5.54 million person years), 14 806 participants with incident cardiovascular disease were identified in the three cohorts. Participants with a higher egg intake had a higher body mass index, were less likely to be treated with statins, and consumed more red meats. Most people consumed between one and less than five eggs per week. In the pooled multivariable analysis, consumption of at least one egg per day was not associated with incident cardiovascular disease risk after adjustment for updated lifestyle and dietary factors associated with egg intake (hazard ratio for at least one egg per day v less than one egg per month 0.93, 95% confidence interval 0.82 to 1.05). In the updated meta-analysis of prospective cohort studies (33 risk estimates, 1 720 108 participants, 139 195 cardiovascular disease events), an increase of one egg per day was not associated with cardiovascular disease risk (pooled relative risk 0.98, 95% confidence interval 0.93 to 1.03, I2=62.3%). Results were similar for coronary heart disease (21 risk estimates, 1 411 261 participants, 59 713 coronary heart disease events; 0.96, 0.91 to 1.03, I2=38.2%), and stroke (22 risk estimates, 1 059 315 participants, 53 617 stroke events; 0.99, 0.91 to 1.07, I2=71.5%). In analyses stratified by geographical location (P for interaction=0.07), no association was found between egg consumption and cardiovascular disease risk among US cohorts (1.01, 0.96 to 1.06, I2=30.8%) or European cohorts (1.05, 0.92 to 1.19, I2=64.7%), but an inverse association was seen in Asian cohorts (0.92, 0.85 to 0.99, I2=44.8%). CONCLUSIONS Results from the three cohorts and from the updated meta-analysis show that moderate egg consumption (up to one egg per day) is not associated with cardiovascular disease risk overall, and is associated with potentially lower cardiovascular disease risk in Asian populations. SYSTEMATIC REVIEW REGISTRATION PROSPERO CRD42019129650.
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9.
Reduction in saturated fat intake for cardiovascular disease.
Hooper, L, Martin, N, Jimoh, OF, Kirk, C, Foster, E, Abdelhamid, AS
The Cochrane database of systematic reviews. 2020;5:CD011737
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UK public health dietary advice focuses on reducing saturated fat intakes and replacing it with polyunsaturated and monounsaturated fats to prevent heart disease. This systematic review of 15 randomised control trials with approximately 59,000 participants aimed to compare the effect of reducing saturated fats and replacing it with polyunsaturated fats, monounsaturated fats, carbohydrate or protein on death or death due to heart disease. The results showed that reducing saturated fat intake for two years did not reduce death or death from heart disease but may have caused a 21% reduction in people suffering a heart attack, stroke or narrowing of the arteries in the arms or legs. Replacing saturated fat with polyunsaturated fat or carbohydrates probably reduces the risk of heart attack, stroke or narrowing of the arteries in the arms and legs, however, there were no effects on death. There was no evidence of any benefits in replacing saturated fat with protein. There was limited evidence on replacement of saturated fats with monounsaturated fats. Overall greater reductions in fat resulted in greater protection from heart disease. It was concluded that the evidence supports replacing saturated fat in the diet to reduce the risk of heart attack, stroke or narrowing of the arteries in the arms and legs, but this may not prevent death. This paper could be used by health care professionals to recommend a low saturated fat diet to reduce heart attack, stroke or narrowing of the arteries in individuals who are at risk or who have already suffered one of these events.
Abstract
BACKGROUND Reducing saturated fat reduces serum cholesterol, but effects on other intermediate outcomes may be less clear. Additionally, it is unclear whether the energy from saturated fats eliminated from the diet are more helpfully replaced by polyunsaturated fats, monounsaturated fats, carbohydrate or protein. OBJECTIVES To assess the effect of reducing saturated fat intake and replacing it with carbohydrate (CHO), polyunsaturated (PUFA), monounsaturated fat (MUFA) and/or protein on mortality and cardiovascular morbidity, using all available randomised clinical trials. SEARCH METHODS We updated our searches of the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE (Ovid) and Embase (Ovid) on 15 October 2019, and searched Clinicaltrials.gov and WHO International Clinical Trials Registry Platform (ICTRP) on 17 October 2019. SELECTION CRITERIA Included trials fulfilled the following criteria: 1) randomised; 2) intention to reduce saturated fat intake OR intention to alter dietary fats and achieving a reduction in saturated fat; 3) compared with higher saturated fat intake or usual diet; 4) not multifactorial; 5) in adult humans with or without cardiovascular disease (but not acutely ill, pregnant or breastfeeding); 6) intervention duration at least 24 months; 7) mortality or cardiovascular morbidity data available. DATA COLLECTION AND ANALYSIS Two review authors independently assessed inclusion, extracted study data and assessed risk of bias. We performed random-effects meta-analyses, meta-regression, subgrouping, sensitivity analyses, funnel plots and GRADE assessment. MAIN RESULTS We included 15 randomised controlled trials (RCTs) (16 comparisons, ~59,000 participants), that used a variety of interventions from providing all food to advice on reducing saturated fat. The included long-term trials suggested that reducing dietary saturated fat reduced the risk of combined cardiovascular events by 21% (risk ratio (RR) 0.79; 95% confidence interval (CI) 0.66 to 0.93, 11 trials, 53,300 participants of whom 8% had a cardiovascular event, I² = 65%, GRADE moderate-quality evidence). Meta-regression suggested that greater reductions in saturated fat (reflected in greater reductions in serum cholesterol) resulted in greater reductions in risk of CVD events, explaining most heterogeneity between trials. The number needed to treat for an additional beneficial outcome (NNTB) was 56 in primary prevention trials, so 56 people need to reduce their saturated fat intake for ~four years for one person to avoid experiencing a CVD event. In secondary prevention trials, the NNTB was 32. Subgrouping did not suggest significant differences between replacement of saturated fat calories with polyunsaturated fat or carbohydrate, and data on replacement with monounsaturated fat and protein was very limited. We found little or no effect of reducing saturated fat on all-cause mortality (RR 0.96; 95% CI 0.90 to 1.03; 11 trials, 55,858 participants) or cardiovascular mortality (RR 0.95; 95% CI 0.80 to 1.12, 10 trials, 53,421 participants), both with GRADE moderate-quality evidence. There was little or no effect of reducing saturated fats on non-fatal myocardial infarction (RR 0.97, 95% CI 0.87 to 1.07) or CHD mortality (RR 0.97, 95% CI 0.82 to 1.16, both low-quality evidence), but effects on total (fatal or non-fatal) myocardial infarction, stroke and CHD events (fatal or non-fatal) were all unclear as the evidence was of very low quality. There was little or no effect on cancer mortality, cancer diagnoses, diabetes diagnosis, HDL cholesterol, serum triglycerides or blood pressure, and small reductions in weight, serum total cholesterol, LDL cholesterol and BMI. There was no evidence of harmful effects of reducing saturated fat intakes. AUTHORS' CONCLUSIONS The findings of this updated review suggest that reducing saturated fat intake for at least two years causes a potentially important reduction in combined cardiovascular events. Replacing the energy from saturated fat with polyunsaturated fat or carbohydrate appear to be useful strategies, while effects of replacement with monounsaturated fat are unclear. The reduction in combined cardiovascular events resulting from reducing saturated fat did not alter by study duration, sex or baseline level of cardiovascular risk, but greater reduction in saturated fat caused greater reductions in cardiovascular events.
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Taurine supplementation for prevention of stroke-like episodes in MELAS: a multicentre, open-label, 52-week phase III trial.
Ohsawa, Y, Hagiwara, H, Nishimatsu, SI, Hirakawa, A, Kamimura, N, Ohtsubo, H, Fukai, Y, Murakami, T, Koga, Y, Goto, YI, et al
Journal of neurology, neurosurgery, and psychiatry. 2019;90(5):529-536
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Mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) is a major clinical entity encompassing mitochondrial diseases resulting from mitochondrial dysfunction. Stroke-like episodes, the most critical symptom of MELAS, are characterised by an abrupt onset of cortical neurological deficits with typical MRI abnormalities not conforming to the distribution of main arteries. The aim of this study was to evaluate the efficacy and safety of high-dose taurine supplementation for prevention of stroke-like episodes. This study is a multicentre, open-label, phase III trial with a total of 291 patients with MELAS. Results show that oral supplementation with high-dose taurine was effective in preventing stroke-like episodes. Furthermore, the 50% responder rate reached 80%, and the annual relapse rate of stroke-like episodes significantly decreased with concomitant increases in blood and cerebrospinal fluid taurine levels. Adverse events associated with taurine were observed among the participants, but no serious adverse events associated with taurine supplementation were reported. Authors conclude that oral high-dose taurine supplementation was effective and safe for the prevention of stroke-like episodes in patients with MELAS by ameliorating the modification defect in the first anticodon nucleotide of mitochondrial tRNA [transfer RNA – a small RNA molecule].
Abstract
OBJECTIVE The aim of this study was to evaluate the efficacy and safety of high-dose taurine supplementation for prevention of stroke-like episodes of MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes), a rare genetic disorder caused by point mutations in the mitochondrial DNA that lead to a taurine modification defect at the first anticodon nucleotide of mitochondrial tRNALeu(UUR), resulting in failure to decode codons accurately. METHODS After the nationwide survey of MELAS, we conducted a multicentre, open-label, phase III trial in which 10 patients with recurrent stroke-like episodes received high-dose taurine (9 g or 12 g per day) for 52 weeks. The primary endpoint was the complete prevention of stroke-like episodes during the evaluation period. The taurine modification rate of mitochondrial tRNALeu(UUR) was measured before and after the trial. RESULTS The proportion of patients who reached the primary endpoint (100% responder rate) was 60% (95% CI 26.2% to 87.8%). The 50% responder rate, that is, the number of patients achieving a 50% or greater reduction in frequency of stroke-like episodes, was 80% (95% CI 44.4% to 97.5%). Taurine reduced the annual relapse rate of stroke-like episodes from 2.22 to 0.72 (P=0.001). Five patients showed a significant increase in the taurine modification of mitochondrial tRNALeu(UUR) from peripheral blood leukocytes (P<0.05). No severe adverse events were associated with taurine. CONCLUSIONS The current study demonstrates that oral taurine supplementation can effectively reduce the recurrence of stroke-like episodes and increase taurine modification in mitochondrial tRNALeu(UUR) in MELAS. TRIAL REGISTRATION NUMBER UMIN000011908.