115 results on '"Lechner, Katharina"'
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102. Modified vaccinia virus Ankara delivers a robust surrogate marker for immune monitoring to sarcoma cells even if cells are being exposed to chemotherapy and heat treatment
- Author
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Tschoep-Lechner, Katharina, primary, Drexler, Ingo, additional, Hammer, Doreen, additional, Neumann, Daniel, additional, Pohla, Heike, additional, Sutter, Gerd, additional, Noessner, Elfriede, additional, and Issels, Rolf-Dieter, additional
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- 2012
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103. Your athlete-patient has a high coronary artery calcification score-'Heart of Stone'. What should you advise? Is exercise safe?
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Lechner, Katharina, Spanier, Bianca, Lechner, Benjamin, and Scherr, Johannes
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CORONARY artery calcification ,ATHLETES ,ATHEROSCLEROTIC plaque ,PHYSICIANS ,CORONARY artery disease ,PROGNOSIS ,MEDICAL research - Published
- 2021
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104. Gemcitabine and cisplatin combined with regional hyperthermia as second-line treatment in patients with gemcitabine-refractory advanced pancreatic cancer.
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Tschoep-Lechner, Katharina Elisabeth, Milani, Valeria, Berger, Frank, Dieterle, Nelli, Abdel-Rahman, Sultan, Salat, Christoph, and Issels, Rolf-Dieter
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CISPLATIN , *PANCREATIC cancer treatment , *DISEASE progression , *TOXICITY testing , *CANCER chemotherapy , *THERAPEUTICS , *THERMOTHERAPY - Abstract
Purpose: There is no standard second-line therapy for patients with advanced pancreatic cancer (APC) after gemcitabine (G) failure. Cisplatin (Cis)-based chemotherapy has shown activity in APC. It is proven that cytotoxicity of G and Cis is enhanced by heat exposure at 40° to 42°C. Therefore G plus Cis with regional hyperthermia (RHT) might be beneficial for patients with G-refractory APC. Patients and methods: We retrospectively analysed 23 patients with advanced ( n = 2) or metastatic ( n = 21) pancreatic cancer with relapse after G mono first-line chemotherapy ( n = 23). Patients had received G (day 1, 1000 mg/m2) and Cis (day 2 and 4, 25 mg/m2) in combination with RHT (day 2 and 4, 1 h) biweekly for 4 months. We analysed feasibility, toxicity, time to second progression (TTP2), overall survival (OS) and clinical response. Results: Between October 1999 and August 2008 23 patients were treated. Haematological toxicity was low with no grade 4 event. Hyperthermia-associated toxicity consisted of discomfort because of bolus pressure (3%), power-related pain (7%) or position-related pain (17%). Median TTP1 was 5.9 months (95% confidence interval (CI): 2.6-9.2), median TTP2 was 4.3 months (95%CI: 1.2-7.4) and OS 12.9 months (95%CI: 9.9-15.9). The disease control rate in 16 patients with available CT scans was 50%. Conclusion: We show first clinical data of G plus Cis with RHT being clinically active in G-pretreated APC with low toxicity. A prospective controlled phase II second-line clinical trial (EudraCT: 2005-003855-11) and a randomised phase III adjuvant clinical trial offering this treatment (HEAT; EudraCT: 2008-004802-14) are currently open for recruitment. [ABSTRACT FROM AUTHOR]
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- 2013
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105. Dispvtatio Theologica De Ivre Et Ivstitia
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Lechner, Katharina
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Quam sub Præsidio R. P. Gasparis Lechneri ... ; conscripsit & defendendam suscepit M. Ioannes Kraus ..., M. DC. XXVII. Ivnii, Dissertation Universität Dillingen 1627, Aus dem Vorbesitz des Klosters Rheinau
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- 1626
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106. Lifestyle factors and high-risk atherosclerosis: Pathways and mechanisms beyond traditional risk factors
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Ronald M. Krauss, Benjamin Lechner, Clemens von Schacky, Martin Halle, Amy L. McKenzie, Johannes Scherr, Uwe Nixdorff, Nicolle Kränkel, Katharina Lechner, Nicolai Worm, University of Zurich, and Lechner, Katharina
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Aging ,Epidemiology ,Vulnerability ,Adipose tissue ,610 Medicine & health ,adipose tissue phenotype ,030204 cardiovascular system & hematology ,Cardiovascular ,Bioinformatics ,Affect (psychology) ,Risk Assessment ,Full Research Paper ,2705 Cardiology and Cardiovascular Medicine ,03 medical and health sciences ,CVD Risk Factors ,0302 clinical medicine ,Risk Factors ,Humans ,2.1 Biological and endogenous factors ,Medicine ,Healthy Lifestyle ,030212 general & internal medicine ,Aetiology ,Life Style ,Nutrition ,business.industry ,novel lifestyle risk factors ,Prevention ,Stressor ,Cardiorespiratory fitness ,Protective Factors ,Risk factor (computing) ,Atherosclerosis ,n-3 fatty acids ,ddc ,Residual risk ,Sleep deprivation ,Good Health and Well Being ,Heart Disease Risk Factors ,Atherosclerotic cardiovascular disease ,plaque phenotype ,10046 Balgrist University Hospital, Swiss Spinal Cord Injury Center ,ketone body ß-hydroxybutyrate ,Patient Safety ,medicine.symptom ,Cardiology and Cardiovascular Medicine ,business ,Risk Reduction Behavior ,2713 Epidemiology - Abstract
Despite major efforts to reduce atherosclerotic cardiovascular disease (ASCVD) burden with conventional risk factor control, significant residual risk remains. Recent evidence on non-traditional determinants of cardiometabolic health has advanced our understanding of lifestyle–disease interactions. Chronic exposure to environmental stressors like poor diet quality, sedentarism, ambient air pollution and noise, sleep deprivation and psychosocial stress affect numerous traditional and non-traditional intermediary pathways related to ASCVD. These include body composition, cardiorespiratory fitness, muscle strength and functionality and the intestinal microbiome, which are increasingly recognized as major determinants of cardiovascular health. Evidence points to partially overlapping mechanisms, including effects on inflammatory and nutrient sensing pathways, endocrine signalling, autonomic function and autophagy. Of particular relevance is the potential of low-risk lifestyle factors to impact on plaque vulnerability through altered adipose tissue and skeletal muscle phenotype and secretome. Collectively, low-risk lifestyle factors cause a set of phenotypic adaptations shifting tissue cross-talk from a proinflammatory milieu conducive for high-risk atherosclerosis to an anti-atherogenic milieu. The ketone body ß-hydroxybutyrate, through inhibition of the NLRP-3 inflammasome, is likely to be an intermediary for many of these observed benefits. Adhering to low-risk lifestyle factors adds to the prognostic value of optimal risk factor management, and benefit occurs even when the impact on conventional risk markers is discouragingly minimal or not present. The aims of this review are (a) to discuss novel lifestyle risk factors and their underlying biochemical principles and (b) to provide new perspectives on potentially more feasible recommendations to improve long-term adherence to low-risk lifestyle factors.
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- 2019
107. Your athlete-patient has a high coronary artery calcification score-'Heart of Stone'. What should you advise? Is exercise safe?
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Johannes Scherr, Benjamin Lechner, Bianca Spanier, Katharina Lechner, University of Zurich, and Lechner, Katharina
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medicine.medical_specialty ,Heart disease ,Sports medicine ,Physical fitness ,Physical Therapy, Sports Therapy and Rehabilitation ,610 Medicine & health ,Disease ,Coronary Artery Disease ,Lower risk ,03 medical and health sciences ,0302 clinical medicine ,2732 Orthopedics and Sports Medicine ,Internal medicine ,medicine ,Humans ,Orthopedics and Sports Medicine ,cardiovascular diseases ,030212 general & internal medicine ,3612 Physical Therapy, Sports Therapy and Rehabilitation ,Exercise ,Coronary atherosclerosis ,Subclinical infection ,business.industry ,Heart ,030229 sport sciences ,General Medicine ,medicine.disease ,Blood pressure ,Athletes ,10046 Balgrist University Hospital, Swiss Spinal Cord Injury Center ,business - Abstract
Coronary artery calcification (CAC) is a strong marker of subclinical coronary atherosclerosis and leading authorities recommend CAC scoring to help inform patient management decisions in cardiovascular disease (CVD) prevention.1 2 This will result in an increasing number of athlete-patients with subclinical coronary atherosclerosis presenting to sport and exercise medicine physicians, raising questions about exercise recommendations in this subgroup. With a specific focus on the recent outcomes data of DeFina and colleagues3 we extend our recent discussion of the topic2 by focusing on how to manage athlete-patients with elevated CAC in the sport and exercise medicine setting. A breakthrough in reporting the association of CAC and mortality risk across different activity levels came from a recent study of 21 758 healthy male participants without prevalent CVD. Higher levels of leisure-time physical activity were associated with a lower risk of mortality at any given level of CAC.3 The authors reported a higher risk metabolic profile (ie, higher baseline blood pressure, higher glucose concentrations and higher triglycerides) in the high volume exercise group with elevated CAC ≥100 AU …
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- 2020
108. Exercise recommendations in athletes with coronary artery calcification
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Martin Halle, Johannes Scherr, Katharina Lechner, Jonathan A. Drezner, University of Zurich, and Lechner, Katharina
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medicine.medical_specialty ,Computed Tomography Angiography ,Epidemiology ,MEDLINE ,610 Medicine & health ,Coronary Artery Disease ,Coronary Angiography ,Risk Assessment ,2705 Cardiology and Cardiovascular Medicine ,Text mining ,Predictive Value of Tests ,Risk Factors ,Internal medicine ,medicine ,Humans ,Vascular Calcification ,Exercise ,Computed tomography angiography ,medicine.diagnostic_test ,biology ,business.industry ,Athletes ,Coronary arteriosclerosis ,Cardiovascular Agents ,Protective Factors ,Prognosis ,biology.organism_classification ,Death, Sudden, Cardiac ,Predictive value of tests ,Coronary artery calcification ,Cardiology ,10046 Balgrist University Hospital, Swiss Spinal Cord Injury Center ,Cardiology and Cardiovascular Medicine ,Risk assessment ,business ,Risk Reduction Behavior ,2713 Epidemiology - Published
- 2019
109. [Cardiovascular manifestations of COVID-19].
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Dutsch A, Lechner K, and Schunkert H
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- Humans, Risk Factors, COVID-19 complications, Cardiovascular Diseases virology
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- 2021
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110. Impact of a 2-year trial of nutritional ketosis on indices of cardiovascular disease risk in patients with type 2 diabetes.
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Athinarayanan SJ, Hallberg SJ, McKenzie AL, Lechner K, King S, McCarter JP, Volek JS, Phinney SD, and Krauss RM
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- Biomarkers blood, Carotid Artery Diseases blood, Carotid Artery Diseases diagnostic imaging, Carotid Artery Diseases etiology, Carotid Intima-Media Thickness, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 diagnosis, Dyslipidemias blood, Dyslipidemias diagnosis, Dyslipidemias etiology, Heart Disease Risk Factors, Humans, Lipoproteins, LDL blood, Nutritive Value, Risk Assessment, Time Factors, Treatment Outcome, Carotid Artery Diseases prevention & control, Diabetes Mellitus, Type 2 diet therapy, Diet, Carbohydrate-Restricted adverse effects, Dyslipidemias prevention & control, Ketosis, Nutritional Status
- Abstract
Background: We have previously reported that in patients with type 2 diabetes (T2D) consumption of a very low carbohydrate diet capable of inducing nutritional ketosis over 2 years (continuous care intervention, CCI) resulted in improved body weight, glycemic control, and multiple risk factors for cardiovascular disease (CVD) with the exception of an increase in low density lipoprotein cholesterol (LDL-C). In the present study, we report the impact of this intervention on markers of risk for atherosclerotic cardiovascular disease (CVD), with a focus on lipoprotein subfraction particle concentrations as well as carotid-artery intima-media thickness (CIMT)., Methods: Analyses were performed in patients with T2D who completed 2 years of this study (CCI; n = 194; usual care (UC): n = 68). Lipoprotein subfraction particle concentrations were measured by ion mobility at baseline, 1, and 2 years and CIMT was measured at baseline and 2 years. Principal component analysis (PCA) was used to assess changes in independent clusters of lipoprotein particles., Results: At 2 years, CCI resulted in a 23% decrease of small LDL IIIb and a 29% increase of large LDL I with no change in total LDL particle concentration or ApoB. The change in proportion of smaller and larger LDL was reflected by reversal of the small LDL subclass phenotype B in a high proportion of CCI participants (48.1%) and a shift in the principal component (PC) representing the atherogenic lipoprotein phenotype characteristic of T2D from a major to a secondary component of the total variance. The increase in LDL-C in the CCI group was mainly attributed to larger cholesterol-enriched LDL particles. CIMT showed no change in either the CCI or UC group., Conclusion: Consumption of a very low carbohydrate diet with nutritional ketosis for 2 years in patients with type 2 diabetes lowered levels of small LDL particles that are commonly increased in diabetic dyslipidemia and are a marker for heightened CVD risk. A corresponding increase in concentrations of larger LDL particles was responsible for higher levels of plasma LDL-C. The lack of increase in total LDL particles, ApoB, and in progression of CIMT, provide supporting evidence that this dietary intervention did not adversely affect risk of CVD.
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- 2020
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111. High-Risk Atherosclerosis and Metabolic Phenotype: The Roles of Ectopic Adiposity, Atherogenic Dyslipidemia, and Inflammation.
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Lechner K, McKenzie AL, Kränkel N, Von Schacky C, Worm N, Nixdorff U, Lechner B, Scherr J, Weingärtner O, and Krauss RM
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- Atherosclerosis diagnosis, Atherosclerosis epidemiology, Atherosclerosis metabolism, Biomarkers metabolism, Cardiometabolic Risk Factors, Cardiovascular Diseases diagnosis, Cardiovascular Diseases epidemiology, Cardiovascular Diseases etiology, Cardiovascular Diseases metabolism, Choristoma complications, Choristoma epidemiology, Choristoma pathology, Dyslipidemias epidemiology, Dyslipidemias metabolism, Dyslipidemias pathology, Humans, Inflammation epidemiology, Inflammation metabolism, Metabolic Syndrome diagnosis, Metabolic Syndrome epidemiology, Metabolic Syndrome metabolism, Obesity complications, Obesity epidemiology, Obesity metabolism, Phenotype, Risk Factors, Adiposity physiology, Atherosclerosis etiology, Dyslipidemias complications, Inflammation complications, Metabolic Syndrome etiology
- Abstract
Current algorithms for assessing risk of atherosclerotic cardiovascular disease (ASCVD) and, in particular, the reliance on low-density lipoprotein (LDL) cholesterol in conditions where this measurement is discordant with apoB and LDL-particle concentrations fail to identify a sizeable part of the population at high risk for adverse cardiovascular events. This results in missed opportunities for ASCVD prevention, most notably in those with metabolic syndrome, prediabetes, and diabetes. There is substantial evidence that accumulation of ectopic fat and associated metabolic traits are markers for and pathogenic components of high-risk atherosclerosis. Conceptually, the subset of advanced lesions in high-risk atherosclerosis that triggers vascular complications is closely related to a set of coordinated high-risk traits clustering around a distinct metabolic phenotype. A key feature of this phenotype is accumulation of ectopic fat, which, coupled with age-related muscle loss, creates a milieu conducive for the development of ASCVD: atherogenic dyslipidemia, nonresolving inflammation, endothelial dysfunction, hyperinsulinemia, and impaired fibrinolysis. Sustained vascular inflammation, a hallmark of high-risk atherosclerosis, impairs plaque stabilization in this phenotype. This review describes how metabolic and inflammatory processes that are promoted in large measure by ectopic adiposity, as opposed to subcutaneous adipose tissue, relate to the pathogenesis of high-risk atherosclerosis. Clinical biomarkers indicative of these processes provide incremental information to standard risk factor algorithms and advanced lipid testing identifies atherogenic lipoprotein patterns that are below the discrimination level of standard lipid testing. This has the potential to enable improved identification of high-risk patients who are candidates for therapeutic interventions aimed at prevention of ASCVD.
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- 2020
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112. The McCAVE Trial: Vanucizumab plus mFOLFOX-6 Versus Bevacizumab plus mFOLFOX-6 in Patients with Previously Untreated Metastatic Colorectal Carcinoma (mCRC).
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Bendell JC, Sauri T, Gracián AC, Alvarez R, López-López C, García-Alfonso P, Hussein M, Miron ML, Cervantes A, Montagut C, Vivas CS, Bessudo A, Plezia P, Moons V, Andel J, Bennouna J, van der Westhuizen A, Samuel L, Rossomanno S, Boetsch C, Lahr A, Franjkovic I, Heil F, Lechner K, Krieter O, and Hurwitz H
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- Antibodies, Monoclonal, Humanized, Antineoplastic Combined Chemotherapy Protocols adverse effects, Bevacizumab adverse effects, Camptothecin therapeutic use, Disease-Free Survival, Fluorouracil adverse effects, Humans, Leucovorin adverse effects, Neoplasm Metastasis, Colorectal Neoplasms drug therapy, Organoplatinum Compounds adverse effects
- Abstract
Background: Bevacizumab, a VEGF-A inhibitor, in combination with chemotherapy, has proven to increase progression-free survival (PFS) and overall survival in multiple lines of therapy of metastatic colorectal cancer (mCRC). The angiogenic factor angiopoetin-2 (Ang-2) is associated with poor prognosis in many cancers, including mCRC. Preclinical models demonstrate improved activity when inhibiting both VEGF-A and Ang-2, suggesting that the dual VEGF-A and Ang-2 blocker vanucizumab (RO5520985 or RG-7221) may improve clinical outcomes. This phase II trial evaluated the efficacy of vanucizumab plus modified (m)FOLFOX-6 (folinic acid (leucovorin), fluorouracil (5-FU) and oxaliplatin) versus bevacizumab/mFOLFOX-6 for first-line mCRC., Patients and Methods: All patients received mFOLFOX-6 and were randomized 1:1 to also receive vanucizumab 2,000 mg or bevacizumab 5 mg/kg every other week. Oxaliplatin was given for eight cycles; other agents were continued until disease progression or unacceptable toxicity for a maximum of 24 months. The primary endpoint was investigator-assessed PFS., Results: One hundred eighty-nine patients were randomized (vanucizumab, n = 94; bevacizumab, n = 95). The number of PFS events was comparable (vanucizumab, n = 39; bevacizumab, n = 43). The hazard ratio was 1.00 (95% confidence interval, 0.64-1.58; p = .98) in a stratified analysis based on number of metastatic sites and region. Objective response rate was 52.1% and 57.9% in the vanucizumab and bevacizumab arm, respectively. Baseline plasma Ang-2 levels were prognostic in both arms but not predictive for treatment effects on PFS of vanucizumab. The incidence of adverse events of grade ≥3 was similar between treatment arms (83.9% vs. 82.1%); gastrointestinal perforations (10.8% vs. 8.4%) exceeded previously reported rates in this setting. Hypertension and peripheral edema were more frequent in the vanucizumab arm., Conclusion: Vanucizumab/mFOLFOX-6 did not improve PFS and was associated with increased rates of antiangiogenic toxicity compared with bevacizumab/mFOLFOX-6. Our results suggest that Ang-2 is not a relevant therapeutic target in first-line mCRC., Implications for Practice: This randomized phase II study demonstrates that additional angiopoietin-2 (Ang-2) inhibition does not result in superior benefit over anti-VEGF-A blockade alone when each added to standard chemotherapy. Moreover, the performed pharmacokinetic and pharmacodynamic analysis revealed that vanucizumab was bioavailable and affected its intended target, thereby strongly suggesting that Ang-2 is not a relevant therapeutic target in the clinical setting of treatment-naïve metastatic colorectal cancer. As a result, the further clinical development of the dual VEGF-A and Ang-2 inhibitor vanucizumab was discontinued., (© 2019 The Authors. The Oncologist published by Wiley Periodicals, Inc. on behalf of AlphaMed Press.)
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- 2020
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113. [Dementia and Metabolic-Vascular Risk Factors: Strategies for Prevention].
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Gonder U, von Schacky C, Worm N, Lechner B, Bock M, and Lechner K
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- Blood Glucose, Diet, Humans, Insulin Resistance, Risk Factors, Cardiovascular Diseases complications, Cardiovascular Diseases epidemiology, Cardiovascular Diseases prevention & control, Dementia complications, Dementia epidemiology, Dementia prevention & control, Metabolic Diseases complications, Metabolic Diseases epidemiology, Metabolic Diseases prevention & control, Risk Reduction Behavior
- Abstract
The prevalence of dementias is on the rise, increases exponentially with age and constitutes a major healthcare burden nationally and worldwide. Dementias are clinically heterogeneous and encompass numerous etiologies. Noteworthy, late onset dementias are closely related to vascular and metabolic risk factors in midlife. Cardiometabolic risk factors commonly precede the onset of cognitive decline for decades. This opens a huge window for prevention. Given the lack of established pharmacological options for treatment of most dementias, preventive strategies are of utmost importance. Several factors have been identified that have the potential to preserve a healthy metabolic phenotype and to attenuate the onset of late onset dementias. Evidence exists for low-risk lifestyle factors including a real food dietary pattern, an adequate supply with long chain omega-3 fatty acids, regular physical activity and restorative sleep, with multimodal concepts showing the greatest cumulative benefit., Competing Interests: NW, BL, MB und KL geben an, dass kein Interessenkonflikt besteht. CvS betreibt Omegametrix, ein Labor zur Fettsäureanalytik. CvS erhielt Honorare für Vorträge und Beratung von BASF/Pronova, Huntsworth Medical, DSM, Marine Ingredients und Norsan. UG erhielt Honorare für Vorträge von Oleofactum und Norsan., (© Georg Thieme Verlag KG Stuttgart · New York.)
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- 2019
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114. [Dietary Recommendations in Metabolic Vascular Syndrome].
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Lechner K, Erickson N, Lechner B, and Horn F
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- Cardiovascular Diseases prevention & control, Dietary Carbohydrates administration & dosage, Dietary Carbohydrates standards, Dietary Fats, Unsaturated administration & dosage, Dietary Fats, Unsaturated standards, Dietary Proteins administration & dosage, Dietary Proteins standards, Feeding Behavior, Fish Products, Humans, Insulin Resistance, Male, Metabolic Syndrome prevention & control, Middle Aged, Non-alcoholic Fatty Liver Disease etiology, Overweight diet therapy, Risk Factors, Cardiovascular Diseases diet therapy, Diet standards, Metabolic Syndrome diet therapy
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Cardiovascular disease is the number one cause of death globally. Poor diet constitutes a key factor in the initiation and progression of cardiovascular disease and has become the leading risk factor for disability and death worldwide. Therefore, addressing suboptimal nutrition is of key prognostic relevance in primary and secondary prevention of metabolic vascular syndrome.Metabolic vascular syndrome is a multidimensional network of acquired cardiometabolic risk factors closely related to insulin resistance (IR) and concomitant hyperinsulinemia. IR, being the underlying cause of metabolic vascular syndrome and certain types of cancer, should attract the attention of every clinician. As changes in lipoprotein metabolism are one of the earliest indicators of metabolic dysfunction, a relevant biomarker for identifying individuals with IR is the TAG/HDL-C ratio.IR - and concomitant metabolic vascular risk - can be effectively treated by lifestyle intervention. If IR is present, dietary carbohydrate restriction has consistently been shown to be superior to dietary fat restriction in reversing metabolic dysfunction. The beneficial effects of carbohydrate restricted diets on metabolic vascular risk are independent of BMI - diet quality therefore confers patient benefit beyond weight reduction.The effect of single nutrients on isolated lipid surrogate markers such as LDL-C does not capture their global effect on metabolic vascular risk.Targeting IR with a low glycemic load, real food diet will reduce overall energy density and will improve all risk factors of metabolic vascular syndrome. In particular, replacing refined carbohydrates with healthy fats in the context of a Mediterranean style-, low carbohydrate and calorie-unrestricted dietary pattern has been shown to significantly reduce burden of metabolic vascular disease., Competing Interests: Disclosure The authors report no conflicts of interest in this work., (© Georg Thieme Verlag KG Stuttgart · New York.)
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- 2017
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115. [Dietary advice for preventing and treating T2DM: A shift of paradigm].
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Lechner K and Parhofer KG
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- Cholesterol, Dietary administration & dosage, Diet, Carbohydrate-Restricted, Humans, Metabolic Syndrome diet therapy, Metabolic Syndrome prevention & control, Diabetes Mellitus, Type 2 diet therapy, Diabetes Mellitus, Type 2 prevention & control, Diet, Diabetic, Diet, Macrobiotic, Dietary Fats administration & dosage
- Published
- 2016
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