Nutr Metab Cardiovasc Dis Research Articles

Relationship between circadian rhythm and Malondialdehyde serum levels in acute and stabilized schizophrenic patients

IntroductionMalondialdehyde (MDA) is a product of polyunsaturated fatty acid peroxidation (Del Rio D, et al. A review of recent studies on MDA as toxic molecule and biological marker of oxidative stress. Nutr Metab Cardiovasc Dis. 2005;15:316-28). It is a biomarker of oxidative stress and is involved in the pathophysiology of schizophrenia (Goh et al. Asian J Psychiatr. 2022;67:102932). Schizofrenia is linked to disrupted oxidative balance and inflammation (Więdłocha et al. Brain Sci. 2023;13:490). Prior research has shown connections between biomarkers and circadian rhythms in schizophrenia (Morera & Abreu. Acta Physiol Scand. 2007;43:313-14) and diabetes type 2 (Kanabrocki EL, et al. Circadian variation in oxidative stress biomarkers in healthy and type II diabetic men. Chronobiol Int. 2002;19:423-39). To determinate if MDA levels have a role in schizophrenia and follow a circadian rhythm may be useful.ObjectivesThe aim of our study is to compare diurnal and nocturnal MDA serum levels in patients in acute and stabilized phases of schizophrenia according to CIE-10 to find out if there are variations related with circadian rhythmsMethods47 patients were included in our study in two clinical phases: acute episode and stabilization. Blood samples were collected at 12:00h and at 00:00h. MDA serum levels were measured twice: when patients were decompensated (admission) and at clinical stabilization (discharge). The relationship between quantitative variables at both times was analysed by T-Student testResultsThere is no significative difference between night and day MDA levels in the acute phase of the schizophrenia (2.22±1.352 vs. 1.93±1.530, p<0.09). There is statistical significance between 12:00 and 00:00 (1.90±1.136 vs. 1.34±0.868, p<0.001) at discharge: it was observed that levels decreased. This result can be interpreted as there is circadian rhythm in stabilized phases.Conclusions MDA levels in patients with schizophrenia do not follow a circadian rhythm in the acute episode. When they are clinically stabilized present a circadian change. These patients lose the circadian rhythm in acute episodes. MDA circadian rhythm may help diagnose the clinical phase and its severity. It is necessary to perform more studies to know its utility as an oxidative biomarkerDisclosure of InterestNone Declared

Lifestyle medicine: a modern medical discipline full of optimism.

British Journal of NursingVol. 32, No. 5 RegularsLifestyle medicine: a modern medical discipline full of optimismEllen Fallows, Alex Maxwell, Rob LawsonEllen FallowsE-mail Address: [email protected]GP and Vice-President, British Society of Lifestyle MedicineSearch for more papers by this author, Alex MaxwellGP and President, British Society of Lifestyle MedicineSearch for more papers by this author, Rob LawsonChair, British Society of Lifestyle MedicineSearch for more papers by this authorEllen Fallows; Alex Maxwell; Rob LawsonPublished Online:13 Mar 2023https://doi.org/10.12968/bjon.2023.32.5.268AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article References Alegría-Torres JA, Baccarelli A, Bollati V. Epigenetics and lifestyle. Epigenomics. 2011;3(3):267-77. https://doi.org/10.2217/epi.11.22 Crossref, Medline, Google ScholarEgger GBinns ARössner SSagner M (eds). Lifestyle medicine: lifestyle, the environment and preventive medicine in health and disease paperback. London: Academic Press; 2017 Google ScholarFurman D, Campisi J, Verdin E et al.. Chronic inflammation in the etiology of disease across the life span. Nat Med. 2019;25(12):1822-1832. https://doi.org/10.1038/s41591-019-0675-0 Crossref, Medline, Google ScholarJacka FN, O’Neil A, Opie R et al.. A randomised controlled trial of dietary improvement for adults with major depression (the ‘SMILES’ trial). BMC Med. 2017;15(1):23. https://doi.org/10.1186/s12916-017-0791-y Crossref, Medline, Google ScholarJarbøl DE, Larsen PV, Gyrd-Hansen D et al.. Determinants of preferences for lifestyle changes versus medication and beliefs in ability to maintain lifestyle changes. A population-based survey. Prev Med Rep. 2017;6:66–73. https://doi.org/10.1016/j.pmedr.2017.02.010 Crossref, Medline, Google ScholarLean ME, Leslie WS, Barnes AC et al.. Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. Lancet. 2018;391(10120):541-551. https://doi.org/10.1016/S0140-6736(17)33102-1 Crossref, Medline, Google ScholarOrnish D. Avoiding revascularization with lifestyle changes: The Multicenter Lifestyle Demonstration Project. Am J Cardiol. 1998;82(10B):72T-76T. https://doi.org/10.1016/s0002-9149(98)00744-9 Crossref, Medline, Google ScholarRidge K (chair). Good for you, good for us, good for everybody. A plan to reduce overprescribing to make patient care better and safer, support the NHS, and reduce carbon emissions. (The report of the National Overprescrining Rreview.) 2021. https://tinyurl.com/3drvj7hu (accessed 1 March 2023) Google ScholarRodriguez-Castaño GP, Caro-Quintero A, Reyes A, Lizcano F. Advances in gut microbiome research, opening new strategies to cope with a western lifestyle. Front Genet. 2017;7:224. https://doi.org/10.3389/fgene.2016.00224 Crossref, Medline, Google ScholarSaneei P, Salehi-Abargouei A, Esmaillzadeh A, Azadbakht L. Influence of Dietary Approaches to Stop Hypertension (DASH) diet on blood pressure: a systematic review and meta-analysis on randomized controlled trials. Nutr Metab Cardiovasc Dis. 2014;24(12):1253-1261. https://doi.org/10.1016/j.numecd.2014.06.008 Crossref, Medline, Google ScholarSrour B, Kordahi MC, Bonazzi E, Deschasaux-Tanguy M, Touvier M, Chassaing B. Ultra-processed foods and human health: from epidemiological evidence to mechanistic insights. Lancet Gastroenterol Hepatol. 2022;7(12):1128-1140. https://doi.org/10.1016/S2468-1253(22)00169-8 Crossref, Medline, Google ScholarTreadwell JS, Wong G, Milburn-Curtis C, Feakins B, Greenhalgh T. GPs’ understanding of the benefits and harms of treatments for long-term conditions: an online survey. BJGP Open. 2020;4(1):bjgpopen20X101016. https://doi.org/10.3399/bjgpopen20X101016 Crossref, Medline, Google Scholar FiguresReferencesRelatedDetails 9 March 2023Volume 32Issue 5ISSN (print): 0966-0461ISSN (online): 2052-2819 Metrics History Published online 13 March 2023 Published in print 9 March 2023 Information© MA Healthcare LimitedPDF download

Commentary: Of women, liver, and heart

This commentary is devoted to a recent study by Ren and Zheng (Nutr Metab Cardiovasc Dis. 2023;33:1349-1357). These authors analyzed sex-stratified long-term outcomes relevant to all-cause and cardiovascular field outcomes among 2,627 nonalcoholic fatty liver disease (NAFLD) adults enrolled in the 2000-2014 National Health and Nutrition Examination Surveys and identified with United States Fatty Liver Index (US FLI) score. Data have shown that, compared to women, men were exposed to a significantly higher all-cause mortality and the maximal risk was seen among those who had obesity and type 2 diabetes. However, women aged ≤ 60 years had a higher risk of death owing to cardiovascular disease (CVD). Conversely, no significantly increased risk of death from CVD was observed among women over 60 years compared to men of the same age group. The study by Ren and Zheng further fosters our understanding of cardiometabolic risk factors, illustrating sex differences present in NAFLD. The distinct impact of NAFLD on CVD by sex and age suggests that cardiometabolic comorbidities may be particularly underestimated among young and middle-aged women with NAFLD. The research by Ren and Zhang may stimulate future investigations exploring the molecular and cellular grounds underlying these findings, notably including the role of fibrosing NAFLD as a strong risk modifier of CVD. In conclusion, an improved understanding of sex-specific regulation of human metabolism in the liver and other key metabolic organs is a research priority finalized for implementing precision medicine approaches in NAFLD arena.

Cardiovascular Harm From Egg Yolk and Meat: More Than Just Cholesterol and Saturated Fat.

Cardiovascular Harm From Egg Yolk and Meat: More Than Just Cholesterol and Saturated Fat.

The inverse association between lipoprotein(a) levels and metabolic syndorome and its components on coronary artery disease patients

Abstract Purpose Neele DM (Diabetologia 1999) showed that insulin suppressed apolipoprotein(a) synthesis by primary cultures of cynomolgus monkey hepatocytes. Therefore, there is a possibility that inverse association exists between lipoprotein(a) [Lp(a)] and metabolic syndorome (Mets) with insulin resistance/hyperinsulinemia for coronary atherosclerosis. Sung KC (Nutr Metab Cardiovasc Dis 2013) described the inverse association between Lp(a) levels and Mets and its components on an asian occupational cohort. And high levels of Lp(a) were associated with preclinical atherosclerosis, as evaluated by coronary calcium score with cardiac computed tomography. There is no similar examination on coronary artery disease (CAD) patients. The purpose is to examine similar considerations on CAD patients. Method 610 subjects with angiographically demonstrated CAD were enrolled. The patients who receiving medication for dyslipidemia and Insulin administration were excluded. The blood samples for laboratory tests were collected after an over night fast. Subjects were divided into four groups according to quartiles of Lp(a) levels (mg/dL). Ranges of quartile groups of Lp(a) were Q1: <9.0, Q2: 9.0–<16.0, Q3: 16.0–<30.0, Q4: ≥30.0. Results The inverse association Lp(a) levels and Mets and its component. The comparison of Q1 (bottom quartile) versus Q4 (top quartile) was shown below; the comorbidity rate of Mets 19.5% versus 8.0% (p<0.01), BMI (kg/m2) 23.5 versus 22.7 (p<0.05), trigyceride (mg/dL) 144.0 versus 107.5 (p<0.0001), HDL cholesterol (mg/dL) 46.8 versus 50.7 (p<0.05), the comorbidity rate of hypertension 60.4% versus 50.7% (p=0.084), glucose (mg/dL) 107.1 versus 100.6 (p<0.05), insulin (μU/mL) 8.49 versus 5.85 (p<0.0001), HOMA-R 2.26 versus 1.44 (p<0.0001). The mean number of diseased coronary vessel was higher in the Q4 group (2.07) than in the Q1 group (1.87) (p<0.05). Conclusion There was the inverse association between Lp(a) levels and Mets and its components on CAD patients. The robust association was found between Lp(a) levels and severity of coronary atherosclerosis despite this inverse correlation. Funding Acknowledgement Type of funding source: None

(PSEUDO)HYPONATREMIA SECONDARY TO LIPOPROTEIN X

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Hyponatremia can be associated with clinically significant disease and often portends worse outcomes, significant hospital morbidity, increased length of stay and hospital cost.[1] Pseudohyponatremia, may be a culprit in overusing hospital resources and unnecessary workup. Here we present a case of altered mental status (AMS) thought initially to be due to hyponatremia. CASE PRESENTATION: A 58 year-old Caucasian male with a history of glioblastoma multiforme (GBM) treated with resection, radiation and temozolomide, on chronic tube feeds (TF) through gastrostomy tube presented with two weeks of AMS. The spouse reported maintenance of TF but was unsure of how much free water she was actually giving. The patient’s exam was significant for blood pressure of 89/60 mmHg, tachycardia at 101 beats per minute, he had lethargy with response to painful stimuli, significant scleral icterus, dry mucous membranes with no gross motor deficits and unremarkable lung and cardiac exams. His workup was significant for sodium of 120 mmol/L, blood urea nitrogen of 48 mg/dL, creatinine of 1.5 mg/dL, direct hyperbilirubinemia of 47 mg/dL (thought to be due to hepatic injury from temozolomide), aspartate aminotransferase of 1,025 U/L, alanine aminotransferase of 595 U/L, alkaline phosphatase of >1,200 U/L, undetectable ammonia level and a negative drug screen. He was started on intravenous fluids and lactulose without any clinical improvement and minimal change in sodium levels. Further workup showed a serum osmolality of 315 mOs/kg (which pointed towards a pseudohyponatremia picture), triglycerides of 343 mg/dL, cholesterol of 1,652 mg/dL, LDL of 24 mg/dL. Full lipoprotein profile and lipid electrophoresis identified lipoprotein X (LpX) which accounted for the observed pseudohyponatremia. MRI head showed possible recurrent GBM without intracranial shift, thought to be the culprit behind his AMS. DISCUSSION: LpX appears in the serum secondary to cholestasis. It is a result of reflux of bile acid into the serum that combines with albumin to form LpX. It is also composed of small amounts of triglycerides, free cholesterol and apolipoprotein C.[2] Interestingly, LpX was not found to be associated with ischemic heart disease. This is thought to be due to a particle size of 18-25 nm, which prevents it from incorporating into the endothelium. It may even be protective against LDL induced atherosclerosis as it decreases LDL oxidation.[3] Thus, lipid lowering medication may not be needed. It is important to note that LpX may cause a hyperviscosity syndrome and could require lipopheresis. CONCLUSIONS: Our case highlights LpX as a rare cause of pseudohyponatremia and the importance of differentiating between true hyponatremia and pseudohyponatremia to avoid unnecessary workup and therapy that may increase morbidity and length of hospital stay. Physicians should be aware of this entity and include it in future practice. Reference #1: Corona G, Giuliani C, Parenti G, et al. The Economic Burden of Hyponatremia: Systematic Review and Meta-Analysis. Am J Med. 2016;129(8):823-835.e4. doi:10.1016/j.amjmed.2016.03.007 Reference #2: Fellin R, Manzato E. Lipoprotein-X fifty years after its original discovery. Nutr Metab Cardiovasc Dis. 2019;29(1):4-8. doi:10.1016/j.numecd.2018.09.006 Reference #3: Chang PY, Lu SC, Su TC, et al. Lipoprotein-X reduces LDL atherogenicity in primary biliary cirrhosis by preventing LDL oxidation. J Lipid Res. 2004;45(11):2116-2122. doi:10.1194/jlr.M400229-JLR200 DISCLOSURES: No relevant relationships by Youssef Abouleish, source=Web Response Speaker/Speaker's Bureau relationship with Genentech Please note: $5001 - $20000 Added 04/01/2020 by Joshua Sill, source=Web Response, value=Honoraria

FRIED FOOD AND POSSIBLE HEALTH HAZARDS

FRIED FOOD AND POSSIBLE HEALTH HAZARDS

Erratum to: Le régime méditerranéen : aliments vedettes ou style alimentaire ? Introduction

19. Knoops KTB, de Groot LCPGM, Kromhout D, et al. (2004) Mediterranean diet, lifestyle factors, and 10-year mortality in elderly european men and women: the hale project. JAMA 292:1433–9 20. Mitrou PN, Kipnis V, Thiebaut ACM, et al. (2007) Mediterranean dietary pattern and prediction of all-cause mortality in a us population: results from the nih-aarp diet and health study. Arch Intern Med 167:2461–8 21. Menotti A, Alberti-Fidanza A, Fidanza F (2012) The association of the mediterranean adequacy index with fatal coronary events in an italian middle-aged male population followed for 40 years. Nutr Metab Cardiovasc Dis 22:369–75 22. Lopez-Garcia E, Rodriguez-Artalejo F, Li TY, et al. (2014) The mediterranean-style dietary pattern and mortality among men and women with cardiovascular disease. Am J Clin Nutr 99:172–80 23. Estruch R, Ros E, Salas-Salvado J, et al. (2013) Primary prevention of cardiovascular disease with a mediterranean diet. N Engl J Med 368:1279–90 24. Pitsavos C, Panagiotakos DB, Tzima N, et al. (2005) Adherence to the mediterranean diet is associated with total antioxidant capacity in healthy adults: the attica study. Am J Clin Nutr 82:694–9 25. Dai J, Jones DP, Goldberg J, et al (2008) Association between adherence to the mediterranean diet and oxidative stress. Am J Clin Nutr 88:1364–70 26. Salas-Salvado J, Garcia-Arellano A, Estruch R, et al. (2008)Components of the mediterranean-type food pattern and serum inflammatory markers among patients at high risk for cardiovascular disease. Eur J Clin Nutr 62:651–9 27. Esposito K, Marfella R, Ciotola M, et al. (2004) Effect of a mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: a randomized trial. JAMA 292:1440–6 28. Marin C, Ramirez R, Delgado-Lista J, et al. (2011) Mediterranean diet reduces endothelial damage and improves the regenerative capacity of endothelium. Am J Clin Nutr 93:267–74 29. Schwingshackl L, Hoffmann G (2014) Mediterranean dietary pattern, inflammation and endothelial function: a systematic review and meta-analysis of intervention trials. Nutr Metab Cardiovasc Dis 24:929–39 30. Ambring A, Johansson M, Axelsen M, et al. (2006) Mediterranean-inspired diet lowers the ratio of serum phospholipid n-6 to n-3 fatty acids, the number of leukocytes and platelets, and vascular endothelial growth factor in healthy subjects. Am J Clin Nutr 83:575–81 31. Garcia-Calzon S, Gea A, Razquin C, et al. (2014) Longitudinal association of telomere length and obesity indices in an intervention study with a mediterranean diet: the predimed-navarra trial. Int J Obes (Lond) 38:177–82 32. Mezzano D, Leighton F, Martinez C, et al. (2001) Complementary effects of mediterranean diet and moderate red wine intake on haemostatic cardiovascular risk factors. Eur J Clin Nutr 55:444–51 33. Lapointe A, Goulet J, Couillard C, et al. (2005) A nutritional intervention promoting the mediterranean food pattern is associated with a decrease in circulating oxidized ldl particles in healthy women from the quebec city metropolitan area. J Nutr 135:410–5 34. Goulet J, Lapointe A, Lamarche B, et al (2007) Effect of a nutritional intervention promoting the mediterranean food pattern on anthropometric profile in healthy women from the quebec city metropolitan area. Eur J Clin Nutr 61:1293–1300 35. Woo J, Woo KS, Leung SS, et al. (2001) The mediterranean score of dietary habits in chinese populations in four different geographical areas. Eur J Clin Nutr 55:215–20

Enabling people to age well

Nursing and Residential CareVol. 17, No. 6 EditorialEnabling people to age wellLinda NazarkoLinda NazarkoSearch for more papers by this authorLinda NazarkoPublished Online:19 May 2015https://doi.org/10.12968/nrec.2015.17.6.307AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article References NHS England (2014) Patient Safety Alert: Stage One: Warning Risk of death or serious harm from accidental ingestion of potassium permanganate preparations. http://bit.ly/1F43eIj (accessed 8 May 2015) Google ScholarEuropean Arteriosclerosis Society (2015) EAS 2015 Session Report. Changing lifestyle: no more excuses: A report from the EAS-ICCR Joint Session: Changing lifestyle patterns: the challenge for cardiovascular prevention. http://bit.ly/1dSxNqj (accessed 8 May 2015) Google ScholarLarsen RN, Kingwell BA, Sethi P et al. (2014) Breaking up prolonged sitting reduces resting blood pressure in over-weight/obese adults. Nutr Metab Cardiovasc Dis 24: 976–82 Crossref, Google ScholarWorld Health Organization (2015) Ageing well must be a global priority. WHO, Geneva. http://www.who.int/ageing/en/ (accessed 8 May 2015) Google Scholar FiguresReferencesRelatedDetailsCited byInfluencing subjective well-being for business and sustainable development using big data and predictive regression analysisJournal of Business Research, Vol. 131 2 June 2015Volume 17Issue 6ISSN (print): 1465-9301ISSN (online): 2052-2932 Metrics History Published online 19 May 2015 Published in print 2 June 2015 Information© MA Healthcare LimitedPDF download

Serum bilirubin levels and risk of prediabetes in young and healthy adults

Inflammation and oxidative stress have been implicated in the development of diabetes mellitus, which is one of the leading risk factors for cardiovascular diseases [ 1 Nolan C.J. Damm P. Prentki M. Type 2 diabetes across generations: from pathophysiology to prevention and management. Lancet. Jul 9 2011; 378: 169-181 Abstract Full Text Full Text PDF PubMed Scopus (643) Google Scholar , 2 Shoelson S.E. Lee J. Goldfine A.B.. Inflammation and insulin resistance. J Clin Invest. Jul 2006; 116: 1793-1801 Crossref PubMed Scopus (84) Google Scholar , 3 Houstis N. Rosen E.D. Lander E.S. Reactive oxygen species have a causal role in multiple forms of insulin resistance. Nature. Apr 13 2006; 440: 944-948 Crossref PubMed Scopus (1927) Google Scholar , 4 Meigs J.B. Larson M.G. Fox C.S. Keaney Jr., J.F. Vasan R.S. Benjamin E.J. Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study. Diabetes Care. Oct 2007; 30: 2529-2535 Crossref PubMed Scopus (176) Google Scholar ]. In this context, the antioxidant and anti-inflammatory effects of bilirubin, a breakdown product of the hemoglobin catabolism, have been increasingly recognized in recent years [ 5 Stocker R. Yamamoto Y. Mcdonagh A.F. Glazer A.N. Ames B.N. Bilirubin is an antioxidant of possible physiological importance. Science. Feb 27 1987; 235: 1043-1046 Crossref PubMed Scopus (2890) Google Scholar , 6 Tomaro M.L. Batlle A.M. Bilirubin: its role in cytoprotection against oxidative stress. Int J Biochem Cell Biol. Mar 2002; 34: 216-220 Crossref PubMed Scopus (119) Google Scholar ]. Serum bilirubin concentrations appear to be inversely related to cardiovascular risk factors [ 7 Oda E. Bilirubin is negatively associated with A1C independently of fasting plasma glucose, age, obesity, inflammation, hemoglobin, and iron in apparently healthy Japanese men and women. Diabetes Care. Oct 2010; 33: e131 Crossref PubMed Scopus (11) Google Scholar , 8 Choi S.H. Yun K.E. Choi H.J. Relationships between serum total bilirubin levels and metabolic syndrome in Korean adults. Nutr Metab Cardiovasc Dis. Jan 2013; 23: 31-37 Abstract Full Text Full Text PDF PubMed Scopus (72) Google Scholar ], and have been associated with improved insulin sensitivity in animal models [ [8] Choi S.H. Yun K.E. Choi H.J. Relationships between serum total bilirubin levels and metabolic syndrome in Korean adults. Nutr Metab Cardiovasc Dis. Jan 2013; 23: 31-37 Abstract Full Text Full Text PDF PubMed Scopus (72) Google Scholar ].

Is Plasma Pentadecanoic Acid a Reasonable Biomarker of Dairy Consumption?

Despite advances in biomedical research and clinical medicine, the burden of cardiovascular disease (CVD) remains extremely high.[1][1] This underscores the importance of primary prevention and the search for novel therapeutic strategies. Modifiable lifestyle factors, including dietary habits, play

Pigment epithelium-derived factor (PEDF) blocks advanced glycation end products (AGEs)-RAGE-induced suppression of adiponectin mRNA level in adipocytes by inhibiting NADPH oxidase-mediated oxidative stress generation

[1] HajjarV,Depta JP,MountisM.DoesvitaminDdeficiencyplaya role in thepathogenesis of chronic heart failure? Do supplements improve survival? Cleveland Clinic. J Med 2010;77:290–3. [2] Pittas AG, ChungM, Trikalinos T, Mitri J, Brendel M, Patel K, et al. Systematic review: vitamin D and cardiometabolic outcomes. Ann Intern Med 2010;152:307–14. [3] Anderson JL, May HT, Horne BD, Bair TL, Hall NL, Carlquist JF, et al. Relation of vitamin D deficiency to cardiovascular risk factors, disease status, and incident events in a general healthcare population. Am J Cardiol 2010;106:963–8. [4] Kim DH, Sabour S, Sagar UN, Adams S, Whellan DJ. Prevalence of hipovitaminosis D in cardiovascular diseases (from the National Health and Nutrition Examination Survey 2001 to 2004). Am J Cardiol 2008;102:1540–4. [5] Ameri P, Ronco D, Casu M, Denegri A, Bovio M, Menoni S, et al. High prevalence of vitamin D deficiency and its association with left ventricular dilation. An echocardiography study in elderly patients with chronic heart failure. Nutr Metab Cardiovasc Dis 2010;20(9):633–40. [6] Fiscella K, Franks P. Vitamin D, race, and cardiovascular mortality: findings from a National US Sample. Ann Fam Med 2010;8:11–8.

Epicardial fat thickness and coronary artery disease correlate independently of obesity

We know that echocardiographic epicardial fat thickness reflects visceral and myocardial fat accumulation [ 1 Iacobellis G. Willens H. Echocardiographic epicardial fat: a review of research and clinical applications. J Am Soc Echocardiogr. 2009; 23: 1311-1319 Abstract Full Text Full Text PDF Scopus (475) Google Scholar , 2 Iacobellis G. Ribaudo M.C. Assael F. et al. Echocardiographic epicardial adipose tissue is related to anthropometric and clinical parameters of metabolic syndrome: a new indicator of cardiovascular risk. J Clin Endocrinol Metab. 2003; 88: 5163-5168 Crossref PubMed Scopus (653) Google Scholar , 3 Malavazos A.E. Di Leo G. Secchi F. et al. Relation of echocardiographic epicardial fat thickness and myocardial fat. Am J Cardiol. 2010; 105: 1831-1835 Abstract Full Text Full Text PDF PubMed Scopus (96) Google Scholar ] and is closely associated with cardiovascular and metabolic risk factors, as previously published in the International Journal of Cardiology [ 4 Iacobellis G. Barbaro G. Gerstein H.C. Relationship of epicardial fat thickness and impaired fasting glucose. Int J Cardiol. 2008; 128: 424-426 Abstract Full Text Full Text PDF PubMed Scopus (77) Google Scholar , 5 Iacobellis G. Singh N. Leonetti F. Sharma A.M. Relationship of epicardial adipose tissue with atrial dimensions and diastolic function in morbidly obese subjects. Int J Cardiol. 2007; 115: 272-273 Abstract Full Text Full Text PDF PubMed Scopus (162) Google Scholar , 6 Malavazos A.E. Ermetic F. Coman C. Corsi M.M. Morrico0ne L. Ambrosi B. Influence of epicardial adipose tissue and adipocytokine levels on cardiac abnormalities in visceral obesity. Int J Cardiol. 2007; 121: 132-134 Abstract Full Text Full Text PDF PubMed Scopus (70) Google Scholar ]. Interestingly, epicardial fat thickness has been also associated with coronary artery disease (CAD) [ 7 Ahn S.G. Lim H.S. Joe D.Y. Kang S.J. Choi B.J. Choi S.Y. Relationship of epicardial adipose tissue by echocardiography to coronary artery disease. Heart. Mar 2008; : 94 Google Scholar , 8 Jeong J.W. Jeong M.H. Yun K.H. Oh S.K. Park E.M. Kim Y.K. Echocardiographic epicardial fat thickness and coronary artery disease. Circ J. 2007; 71: 536-539 Crossref PubMed Scopus (283) Google Scholar , 9 Eroglu S. Sade L.E. Yildirir A. et al. Epicardial adipose tissue thickness by echocardiography is a marker for the presence and severity of coronary artery disease. Nutr Metab Cardiovasc Dis. 2009; 19: 211-217 Abstract Full Text Full Text PDF PubMed Scopus (195) Google Scholar , 10 Sade L.E. Eroglu S. Bozbaş H. et al. Relation between epicardial fat thickness and coronary flow reserve in women with chest pain and angiographically normal coronary arteries. Atherosclerosis. 2009; 204: 580-585 Abstract Full Text Full Text PDF PubMed Scopus (121) Google Scholar ]. However, we do not know whether this association is explained by the concurrence of obesity or by an independent effect of epicardial fat. This study was aimed to address to this question.

Association of Increased Plasma Cardiotrophin-1 With Left Ventricular Mass Indexes in Normotensive Morbid Obesity

To the Editor: We read with great interest the article by Lopez et al,1 who hypothesize that cardiotrophin-1 (CT-1), a cytokine that induces cardiomyocyte growth, may be abnormally upregulated in hypertensive patients with inappropriate left ventricular mass (LVM), suggesting that an excess of CT-1 may contribute to inappropriate left ventricular growth. This possibility is supported by the finding of a correlation between CT-1 levels and the observed LVM/predicted LVM ratio, independent from concentric left ventricular hypertrophy (LVH). de Simone et al2 suggested that, other than hemodynamic load, the process that yields to inappropriate LVH can also depend on the protracted activity over time of cytokines, among other nonhemodynamic factors. The observation by Lopez et al1 that CT-1 levels were high in treated patients in whom inappropriate LVM persisted …

Cardiac involvement in children with coeliac disease and the effect of gluten free diet on cardiac performance

Background. The association between coeliac disease (CD) and several other disorders is well established [ [1] Dewar D.H. Clinical features and diagnosis of celiac disease. Gastroenterology. 2005; 128: S19-S24 Abstract Full Text Full Text PDF PubMed Scopus (185) Google Scholar ]. Idiopathic dilated cardiomyopathy and autoimmune myocarditis have been recently described in association with or as a presenting feature of CD in adult [ 2 Curione M. Carnitine deficiency in patients with celiac disease and idiopathic dilated cardiomyiopathy. Nutr Metab Cardiovasc Dis. 2005; 15: 279-283 Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar , 3 Frustaci A. Celiac disease associated with autoimmune myocarditis. Circulation. 2002; 105: 2611-2618 Crossref PubMed Scopus (152) Google Scholar ]. No evidence-based data is available for this issue in children.

Soy Protein, Isoflavones, and Cardiovascular Health

This editorial summarizes the recent American Heart Association (AHA) Science Advisory on soy protein and isoflavones (phytoestrogens) published in the February 21, 2006, issue of Circulation .1 Soy protein and isoflavones have gained considerable attention for their potential role in improving risk factors for cardiovascular disease. This scientific advisory report assesses the more recent work published on soy protein and its component isoflavones. In 22 randomized trials, isolated soy protein with isoflavones compared with milk or other proteins decreased LDL cholesterol concentrations in most studies; the average effect was approximately 3%. This reduction is very small compared with the large amount of soy protein tested in these studies, averaging 50 g, approximately half the usual total daily protein intake. No significant effects were evident on HDL cholesterol, triglycerides, lipoprotein(a), or blood pressure. Among 19 studies of soy isoflavones, the average effect on LDL cholesterol and other lipid risk factors was nil. Soy protein or isoflavones have not been shown to lessen vasomotor symptoms of menopause, and results are mixed regarding slowing of postmenopausal bone loss. The efficacy and safety of soy isoflavones for preventing or treating cancer of the breast, endometrium, and prostate are not established; evidence from clinical trials is meager and cautionary as regards a possible adverse effect. For this reason, use of isoflavone supplements in food or pills is not recommended. Thus, earlier research indicating that soy protein compared with other proteins has clinically important favorable effects has not enjoyed confirmation. In contrast, many soy products should be beneficial to cardiovascular and overall health because of their high content of polyunsaturated fats, fiber, vitamins, and minerals and low content of saturated fat. In October 1999, the US Food and Drug Administration (FDA) approved labeling for foods containing soy protein as protective against coronary heart disease.2 …

Cardiovascular risk assessment based on US cohort studies: findings from a National Heart, Lung, and Blood institute workshop.

This report was derived from a workshop on cardiovascular risk assessment sponsored by the National Heart, Lung, and Blood Institute, which addressed whether risk equations developed in the Framingham Heart Study (FHS) for predicting new-onset coronary heart disease (CHD) apply to diverse population groups. Preparation for the workshop included a reanalysis and comparison of prospective studies in several different populations in which risk factors were related to cardiovascular outcomes. Some studies included fatal and nonfatal CHD end points, whereas others contained only CHD mortality. Extensive collaboration provided as much uniformity as possible with respect to both risk factors and CHD end points. The FHS has led in defining the quantitative impact of risk factors.1 Many potential risk factors were measured and related to cardiovascular outcomes. Several risk factors proved to be strong, largely independent predictors of cardiovascular disease (CVD). These factors—advancing age, cigarette smoking, blood pressure (particularly systolic), cholesterol in total serum and HDL, and diabetes—served as the basis for the development of risk prediction equations.1 If FHS risk estimates are to be widely used, they must apply widely in the US population. To document their transportability, they must be compared with prospective studies in other populations. Although the FHS is the longest running prospective study, there are other major studies. The cardiovascular end points of these other studies have varied. Some include cardiovascular morbidity and mortality; others have only cardiovascular mortality. Among the end points, CHD is the most extensively reported; for this reason, CHD was the primary focus of the workshop. ### Multivariate Relative Risk Comparisons In preparation for the workshop, multivariate regression coefficients for each risk factor were compared in different populations with those of the FHS. Adjusted relative risk estimates make it possible to determine whether each independent risk factor confers a similar or different relative risk among different …

Association of Sociodemographic Factors with Barriers Reported by Patients Receiving Nutrition Counseling as Part of Cardiac Rehabilitation

Nutrition education is an important part of cardiac rehabilitation programs ( (1) Travers K.D. Tan M.H. McCleave A.P. Murphy A. Whiting S. Evaluation of a motivational education program for cardiovascular risk reduction effects on knowledge and behavior. J Nutr Educ. 1992; 24: 109-115 Google Scholar , (2) Karvetti R-.L. Hämäläinen H. Long-term effects of nutrition education on myocardial infarction patients a 10-year follow-up study. Nutr Metab Cardiovasc Dis. 1993; 3: 185-192 Google Scholar ). The nutritional aims of Finnish cardiac rehabilitation programs are to effect permanent, favorable changes in diet, nutrient intake, and serum lipid levels. Similar recommendations are part of cardiac rehabilitation programs in the United States ( (3) Wenger N.K. Froelicher E.S. Smith L.K. Ades P.A. Berra K. Blumenthal J.A. Certo C.M.E. Dattilo A.M. Davis D. DeBusk R.F. Drozda Jr, J.P. Fletcher B.J. Franklin B.A. Gaston H. Greenland P. McBride P.E. McGregor C.G.A. Oldridge N.B. Piscatella J.C. Rogers F.J. Cardiac Rehabilitation as Secondary Prevention. Clinical Practice Guideline Quick Reference Guide for Clinicians, No. 17. US Dept of Health and Human Service, Public Health Service, Agency for Health Care Policy and Research and National Heart, Lung, and Blood Institute, Rockville, Md1995 Google Scholar ). Nutrition education has only limited value, however, if patients do not follow the advice.