Effect of the Mediterranean diet on heart failure biomarkers: a randomized sample from the <scp>PREDIMED</scp> trial

Fitó, Montserrat; Estruch, Ramón; Salas‐Salvadó, Jordi; Martínez‐González, Miguel Ángel; Arós, Fernando; Vila, Joan; Corella, Dolores; Díaz, Oscar; Sáez, Guillermo T.; Torre, Rafael de la; Mitjavila, MT; Muñoz, Miguel Ángel; Lamuela‐Raventós, Rosa M.; Ruı́z-Gutı́errez, Valentina; Fiol, Miquel; Gómez‐Gracia, Enrique; Lapetra, José; Ros, Emilio; Serra‐Majem, Lluís; Covas, Marı́a-Isabel

doi:10.1002/ejhf.61

Cited by 136 publications

(91 citation statements)

References 32 publications

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“…[42][43][44][45][46][47][48][49][50][51][52][53] Mediterranean Diet 975 lower total cholesterol/HDL-C ratios compared with the low(er)-fat group (À0.38 and À0.26, respectively). In addition, the Mediterranean diet with nuts reduced fasting glucose (À5.4 mg/dL), SBP (À7.1 mm Hg), DBP (À2.6 mm Hg), and TG concentrations (À13 mg/dL) relative to the low(er)-fat diet.…”

Section: Mediterranean Diet: Overview and Evidence Basementioning

confidence: 99%

Recent Findings of Studies on the Mediterranean Diet

Richter¹,

Skulas‐Ray²,

Kris-Etherton³

2014

Endocrinology and Metabolism Clinics of North America

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Section: Mediterranean Diet: Overview and Evidence Basementioning

confidence: 99%

Recent Findings of Studies on the Mediterranean Diet

Richter¹,

Skulas‐Ray²,

Kris-Etherton³

2014

Endocrinology and Metabolism Clinics of North America

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“…It has been shown to prevent cardiovascular events. 323 The PREDIMED study (Prevención con Dieta Mediterránea), a multicenter, randomized trial to assess the effects of the Mediterranean diet (components listed in Table 12) on the primary prevention of CVD, randomized …”

Section: Dietary Interventions For the Prevention Of Hfmentioning

confidence: 99%

Contributory Risk and Management of Comorbidities of Hypertension, Obesity, Diabetes Mellitus, Hyperlipidemia, and Metabolic Syndrome in Chronic Heart Failure: A Scientific Statement From the American Heart Association

Bozkurt¹,

Aguilar²,

Deswal³

et al. 2016

Circulation

343

220

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CLINICAL STATEMENTS AND GUIDELINESfailed to show a significant reduction of SBP in patients with resistant hypertension. 81 Other strategies such as targeting excessive sympathetic nerve activity by carotid body denervation are awaiting clinical validation in the hypertension and HF populations. Drugs to Avoid in Patients With HFSeveral classes of drugs should be avoided in patients with HFrEF with a history of hypertension. Because of their negative inotropic properties and the increased likelihood of worsening HF symptoms, the nondihydropyridine calcium channel blockers such as diltiazem and verapamil should be avoided. 8 The dihydropyridine calcium channel blocker amlodipine appeared to be safe in patients with severe HFrEF in the PRAISE trial (Prospective Randomized Amlodipine Survival Evaluation), 82 as was felodipine. 73 In the current 2013 HF guidelines, most calcium channelblocking drugs except amlodipine are not recommended. 8Although clonidine is an effective antihypertensive agent, a similar centrally acting drug, moxonidine, was associated with increased mortality in patients with HF; thus, centrally acting norepinephrine-depleting agents may need to be avoided or used with caution in patients with HFrEF. 83In the ALLHAT trial, the α-blocker doxazosin arm of the trial was discontinued because of a 2-fold increase in the risk of developing HF compared with chlorthalidone treatment. 45 Although the ALLHAT study excluded patients with established HF and there are caveats about extrapolating these data to the management of hypertension in patients with established HF, the safety and efficacy of α-blockers in the management of patients with HF with hypertension are currently unclear. Potent direct-acting vasodilators such as minoxidil should also be avoided because of their renin-related salt and fluid-retaining effects. Nonsteroidal anti-inflammatory agents should be used with caution in these patients, given their effects on BP, volume status, and renal function. Treatment of Hypertension in Patients With HF With Preserved LVEFMost patients with HF and preserved LVEF (HFpEF), especially elderly women, have hypertension. A significant proportion of these patients also have evidence of LV hypertrophy, and some may have atrial dilatation, cardiac enlargement, and wall motion abnormalities without LV systolic dysfunction. Patients with HFpEF may respond particularly well to the treatment of hypertension with regression of hypertrophy 84 and improvement in filling pressures. 84,85 Most patients with HFpEF require treatment with cardiac medications for the comorbidities of hypertension, diabetes mellitus, coronary artery disease, and atrial fibrillation. The 2013 HF guidelines suggest that the use of β-blocking agents, ACE inhibitors, and ARBs in patients with hypertension is reasonable to control BP in patients with HFpEF. 8 The use of ARBs might also be considered to decrease hospitalizations for patients with HFpEF. recommendations Harmonized With Existing Guidelines for the recognition and Treatment of pa...

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“…In these studies, a low-fat, high-complex carbohydrate diet with a high-dietary fibre content was advised. Another dietary approach in the prevention of diabetes is the Mediterranean diet, rich in olive oil, which may provide cardiovascular benefits (49) . Manipulation of dietary fat quality by increasing the MUFA content or the n-3 or n-6 long-chain PUFA content of the diet in intervention studies has not shown consistent results on insulin sensitivity (40)(41)(42)(43) .…”

Section: Long-term Dietary Intervention Manipulating Diet Compositionmentioning

confidence: 99%

Characterisation of fatty acid metabolism in different insulin-resistant phenotypes by means of stable isotopes

Blaak

2017

Proc. Nutr. Soc.

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The obese insulin resistant and/or prediabetic state is characterised by systemic lipid overflow, mainly driven by an impaired lipid buffering capacity of adipose tissue, and an impaired capacity of skeletal muscle to increase fat oxidation upon increased supply. This leads to the accumulation of bioactive lipid metabolites in skeletal muscle interfering with insulin sensitivity via various mechanisms. In this review, the contribution of dietary v. endogenous fatty acids to lipid overflow, their extraction or uptake by skeletal muscle as well as the fractional synthetic rate, content and composition of the muscle lipid pools is discussed in relation to the development or presence of insulin resistance and/or an impaired glucose metabolism. These parameters are studied in vivo in man by combining a dual stable isotope methodology with [ 2 H 2 ]-and [U-13 C]-palmitate tracers with the arterio-venous balance technique across forearm muscle and biochemical analyses in muscle biopsies. The insulin-resistant state is characterised by an elevated muscle TAG extraction, despite similar supply, and a reduced skeletal muscle lipid turnover, in particular after intake of a high fat, SFA fat meal, but not after a high fat, PUFA meal. Data are placed in the context of current literature, and underlying mechanisms and implications for long-term nutritional interventions are discussed. The prevalence of overweight and overweight-related metabolic disturbances is increasing at an alarming rate. Worldwide more than 50 % of the adults is overweight (>one billion individuals) and a further 12 % (475 million) can be classified as clinically obese. Every year at least 2·8 million adults die as a result of being overweight/obese (http://www.who.int/gho/ncd/risk_fac-tors/overweight/en). Obesity is an important risk factor for chronic metabolic diseases such as type 2 diabetes mellitus (T2DM) and CVD. A disturbed lipid metabolism in multiple tissues, including adipose tissue, liver, skeletal muscle, gut and pancreas may play an important role in the development of insulin resistance (IR), an impaired glucose metabolism and T2DM. These disturbances, in particular an impaired adipose tissue lipid handling, may lead to systemic lipid overflow, increased circulating concentrations of NEFA and TAG and accumulation of lipids in non-adipose tissues (1)(2)(3)(4) . This lipid overflow together with an impaired capacity to adjust fatty acid (FA) oxidation to FA supply in skeletal muscle (metabolic inflexibility (3) ) may cause excess fat storage in skeletal muscle, which is related to the development or worsening of IR. IR in concert with progressive β-cell failure leads to an increased blood glucose concentration in the non-diabetic range, classified as impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). IFG (fasting glucose >5·6 mM/l) and IGT (2 h oral glucose tolerance testderived glucose concentration >7·8 mM) are intermediate states in the transition from a normal glucose tolerance towards T2DM. IFG and IGT may represent dis...

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Effect of the Mediterranean diet on heart failure biomarkers: a randomized sample from the PREDIMED trial

Cited by 136 publications

References 32 publications

Recent Findings of Studies on the Mediterranean Diet

Recent Findings of Studies on the Mediterranean Diet

Contributory Risk and Management of Comorbidities of Hypertension, Obesity, Diabetes Mellitus, Hyperlipidemia, and Metabolic Syndrome in Chronic Heart Failure: A Scientific Statement From the American Heart Association

Characterisation of fatty acid metabolism in different insulin-resistant phenotypes by means of stable isotopes

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