mitos e verdades sobre dietas da moda - crn-2 · dietas da moda nutr. ms. bruna pontin...

MITOS E VERDADES SOBRE DIETAS DA MODA

Nutr. Ms. Bruna PontinNutricionista Clínica

Profa da Universidade do Vale do Rio dos SinosPesquisadora do Instituto Tecnológico em Alimentos para a Saúde -

itt NUTRIFOR

RESUMO DA PALESTRA

terça-feira, 13 de janeiro de 2015

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POR QUE AINDA HÁ ESPAÇO SOBRE DIETAS DA MODA?

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DIETAS DA MODA:QUAIS AS EVIDÊNCIAS?


RESEARCH

Review

Meets Learning Need Codes 5000, 5110, and 5220

Advances in Celiac Disease and Gluten-Free DietMARY M. NIEWINSKI, MS, RD

ABSTRACTCeliac disease is becoming an increasingly recognizedautoimmune enteropathy caused by a permanent intol-erance to gluten. Once thought to be a rare disease ofchildhood characterized by diarrhea, celiac disease is ac-tually a multisystemic disorder that occurs as a result ofan immune response to ingested gluten in geneticallypredisposed individuals. Screening studies have revealedthat celiac disease is most common in asymptomaticadults in the United States. Although considerable scien-tific progress has been made in understanding celiac dis-ease and in preventing or curing its manifestations, astrict gluten-free diet is the only treatment for celiacdisease to date. Early diagnosis and treatment, togetherwith regular follow-up visits with a dietitian, are neces-sary to ensure nutritional adequacy and to prevent mal-nutrition while adhering to the gluten-free diet for life.The purpose of this review is to provide clinicians withcurrent updated information about celiac disease, its di-verse clinical presentation and increased prevalence, thecomplex pathophysiology and strong genetic predisposi-tion to celiac disease, and its diagnosis. This review fo-cuses in detail on the gluten-free diet and the importanceof intense expert dietary counseling for all patients withceliac disease. Recent advances in the gluten-free dietinclude food allergen labeling as well as the US Food andDrug Administration’s proposed definition of the food-labeling term gluten-free. The gluten-free diet is complex

and patients need comprehensive nutrition educationfrom a skilled dietitian.J Am Diet Assoc. 2008;108:661-672.

Celiac disease is becoming an increasingly recognizeddisorder. This disease is a complex autoimmune en-teropathy caused by a permanent intolerance to glu-ten in genetically susceptible individuals. Gluten is themain storage protein of wheat. The alcohol-soluble frac-tion (prolamin) of gluten, gliadin, is toxic in celiac dis-ease, as are similar proteins in barley (hordein) and rye(secalin) (1). Celiac disease is associated with maldiges-tion and malabsorption of nutrients, vitamins, and min-erals in the gastrointestinal tract. Epidemiological stud-ies in Europe and the United States indicate that celiacdisease is common and that the prevalence of celiac dis-ease is approximately 1% in the general population (2-7).Long delays between onset of symptoms and diagnosisoften occur (8), and the condition remains underdiag-nosed. Currently, the only available treatment is lifelongadherence to a gluten-free diet (4).

CLINICAL PRESENTATIONSamuel Gee, MD, described the classical features of celiacdisease in 1887 as diarrhea, lassitude, and failure tothrive (9). At that time, Gee believed regulation of foodwas the main part of the treatment and noted that thedisease was not age-specific. In 1953, Willem Karel Dickedemonstrated in a controlled study, that wheat, rye, andbarley triggered celiac disease, and that the conditioncould be reversed after their exclusion from the diet (10).The first accurate description of the celiac lesion, how-ever, was by Paulley, in 1954, when he examined full-thickness biopsy specimens taken at laparoscopy from apatient with celiac disease. He described broad flat villiand a dense chronic lymphoepithelial inflammatory cellinfiltrate in the small intestinal mucosa (11). A staging ofmucosal injury, first described by Marsh, demonstratedthe pathological spectrum of celiac disease, and describedthe progression of the abnormalities of the intestinalmucosal response to gluten. Five interrelated lesionshave been characterized that range from minimal injuryof the mucosa with an increase in intraepithelial lympho-cytes to total villous atrophy (12). The classic celiac lesionis characterized by infiltration of lymphocytes in the ep-ithelium and the lamina propria, with crypt hyperplasiaand villous atrophy (12-15).

M. Niewinski is a specialist in nutrition and medicaldietetics in the Department of Pediatrics/Genetics at theUniversity of Illinois at Chicago Medical Center andan adjunct clinical instructor in the Department ofKinesiology and Nutrition at the University of Illinoisat Chicago.

Address correspondence to: Mary M. Niewinski, MS,RD, Department of Pediatric Genetics M/C 856, Univer-sity of Illinois at Chicago, 840 S Wood St, Chicago, IL60612. E-mail: [email protected]

Manuscript accepted: October 15, 2007.Copyright © 2008 by the American Dietetic

Association.0002-8223/08/10804-0012$34.00/0doi: 10.1016/j.jada.2008.01.011

© 2008 by the American Dietetic Association Journal of the AMERICAN DIETETIC ASSOCIATION 661

J Am Diet Assoc. 2008;108:661-672.

Recently, the quality of the gluten-free diet was challenged by Thompson, who rationalized that in the general population, enriched fortified wheat-based cereal products contribute a large percentage to the daily intake of thiamin, riboflavin, niacin, iron, and folic acid. Thompson found that many gluten-free cereal products contain inferior amounts of thiamin, riboflavin, niacin, folate, and iron compared with the enriched wheat products that they are intended to replace.

A recent dietary survey in the United States assessed the diets of adults with celiac disease who were following a strict gluten-free diet. An analysis of 3-day food records suggested inadequate intakes of fiber, iron, and calcium in ~ 50% of females studied.


Gluten-Free Diet: Imprudent Dietary Advice for theGeneral Population?Glenn A. Gaesser, PhD; Siddhartha S. Angadi, PhD

GLUTEN-FREE DIETING HAS GAINED CONSIDERABLEpopularity in the general population.1-3 Between2004 and 2011 the market for gluten-free productsgrew at a compound annual growth rate of 28%,with annual sales expected to reach approximately $2.6 bil-lion in 2012.2 As of April 20, 2012, Amazon.com listed 4,765entries for the topic “gluten-free.” AGoogle search at the sametime for “gluten-free diet” produced more than 4.2 millionresults. The number-one reason consumers cite for buyinggluten-free products is that they are perceived to be healthierthan their gluten-containing counterparts.3 Endorsementsfrom celebrities have undoubtedly contributed to the in-creased awareness of possible health benefits of gluten avoid-ance, including weight loss.4,5

Despite the health claims for gluten-free eating, there is nopublished experimental evidence to support such claims forthe general population. In fact, there are data to suggest thatgluten itself may provide some health benefits, and that glu-ten avoidance may not be justified for otherwise healthy in-dividuals. Our primary purpose is to briefly describe this evi-dence and raise awareness of the potential pitfalls of adoptinga gluten-free diet in persons without diagnosed gluten-re-lated disorders.

INDICATIONS FOR A GLUTEN-FREE DIETGluten is a protein composite consisting of gliadins and glu-tenins, and is found in foods processed from wheat and re-lated grains such as barley and rye. There is a spectrum ofgluten-related disorders, including celiac disease, gluten sen-sitivity, and wheat allergy.1,2 Wheat allergy is an adverse im-munologic reaction specific to wheat proteins.1,2 Prevalenceof documented wheat allergy is quite low, estimated at onlyabout 0.1% of individuals in Westernized countries.1 Becausewheat allergy can be treated with wheat avoidance, a wheat-free diet may be more permissive than a strict gluten-freediet.1 Gluten sensitivity (also referred to as nonceliac gluten

intolerance), is characterized by a heightened immunologicreaction to gluten in genetically susceptible people.6 Clinicaldiagnosis is generally based on responses to a gluten-freediet.1 Common symptoms of gluten sensitivity, such as fa-tigue and headaches, and gastrointestinal distress, includinggas, bloating, and diarrhea, frequently improve with theadoption of a gluten-free diet. The inherent subjectivity indiagnosis and resolutionof these symptoms likely contributesto the popularity of gluten-free diets.Celiac disease is a complex autoimmune enteropathy that

affects the small bowel after ingestion of gluten-containinggrains, includingwheat, rye, and barley, in genetically suscep-tible people.7 Estimated prevalence of celiac disease is ap-proximately 1%.8,9 The disease canmanifest itself in a range ofclinical presentations, including malabsorption syndromeand a spectrum of symptoms affecting multiple target or-gans.10 A strict gluten-free diet is an established remedy forindividuals with celiac disease because it has been shown tolower incidence of related diseases, such as gastrointestinalcancers.7-9,11 Lifelong adherence to a strict gluten-free diet,devoid of proteins from wheat, rye, barley, and related cere-als, remains the gold standard of treatment in celiac dis-ease.7-9

There are some data to suggest that following a gluten-freediet may ameliorate gastrointestinal and/or systemic symp-toms in individuals with systemic lupus erythematosus, der-matitis herpetiformis, irritable bowel syndrome, rheumatoidarthritis, type 1 diabetes, thyroiditis, and psoriasis.12,13 Glu-ten-free diets have also been used by patients with autismspectrum disorders (ASD).2,14 However, there are no defini-tive data to support the use of gluten-free diets in ASD,15 andthe American Academy of Pediatrics does not support the useof gluten-free diets as a primary treatment for individualswith ASD.16

Apart from the demonstrated effectiveness of a gluten-freediet for treating the spectrum of gluten-related disorders andthe conditions mentioned above, evidence-based researchsupporting the merits of a gluten-free diet as a healthier op-tion for the general population is lacking.

GLUTEN-FREE DIET AND WEIGHT LOSS: WHEREIS THE EVIDENCE?Despite the growing popularity of gluten-free diets and celeb-rity endorsements of the merits of a gluten-free diet forweight loss,4,5 there are no published reports showing that agluten-free diet produces weight loss in persons without ce-liac disease or gluten sensitivity. There are a number of stud-ies of patientswith celiac disease that reportedweight changeas an outcome measure following a gluten-free diet.17-19

ARTICLE INFORMATION

Article history:Accepted 29 May 2012

Keywords:WheatGlutenGut microbiotaFructan-type resistant starch

Copyright © 2012 by the Academy of Nutrition and Dietetics.2212-2672/$36.00doi: 10.1016/j.jand.2012.06.009

RESEARCHCommentary

1330 JOURNAL OF THE ACADEMY OF NUTRITION AND DIETETICS © 2012 by the Academy of Nutrition and Dietetics.

J Am Diet Assoc. 2012;112:1330-33.

Apart from the demonstrated effectiveness of a gluten-free diet for treating the spectrum of gluten-related disorders and the conditions mentioned above, evidence-based research supporting the merits of a gluten-free diet as a healthier option for the general population is lacking.


Gluten-free diet reduces adiposity, inflammation and insulin resistance associatedwith the induction of PPAR-alpha and PPAR-gamma expression☆,☆☆

Fabíola Lacerda Pires Soaresa,b,⁎, Rafael de Oliveira Matosob, Lílian Gonçalves Teixeirab, Zélia Menezesc,Solange Silveira Pereiraa,b, Andréa Catão Alvesb, Nathália Vieira Batistad, Ana Maria Caetano de Fariab,

Denise Carmona Carad, Adaliene Versiani Matos Ferreirae, Jacqueline Isaura Alvarez-Leiteb

aDepartamento de Alimentos, Faculdade de Farmácia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, BrazilbDepartamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil

cDepartamento de Fisiologia e Biofísica, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, BrazildDepartamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, BrazileDepartamento de Enfermagem Básica, Escola de Enfermagem, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil

Received 21 March 2012; received in revised form 20 July 2012; accepted 13 August 2012

Abstract

Gluten exclusion (protein complex present in many cereals) has been proposed as an option for the prevention of diseases other than coeliac disease.However, the effects of gluten-free diets on obesity and its mechanisms of action have not been studied. Thus, our objective was to assess whether glutenexclusion can prevent adipose tissue expansion and its consequences. C57BL/6 mice were fed a high-fat diet containing 4.5% gluten (Control) or no gluten (GF).Body weight and adiposity gains, leukocyte rolling and adhesion, macrophage infiltration and cytokine production in adipose tissue were assessed. Blood lipidprofiles, glycaemia, insulin resistance and adipokines were measured. Expression of the PPAR-α and γ, lipoprotein lipase (LPL), hormone sensitive lipase (HSL),carnitine palmitoyl acyltransferase-1 (CPT-1), insulin receptor, GLUT-4 and adipokines were assessed in epidydimal fat. Gluten-free animals showed a reductionin body weight gain and adiposity, without changes in food intake or lipid excretion. These results were associated with up-regulation of PPAR-α, LPL, HSL andCPT-1, which are related to lipolysis and fatty acid oxidation. There was an improvement in glucose homeostasis and pro-inflammatory profile-relatedoverexpression of PPAR-γ. Moreover, intravital microscopy showed a lower number of adhered cells in the adipose tissue microvasculature. The overexpressionof PPAR-γ is related to the increase of adiponectin and GLUT-4. Our data support the beneficial effects of gluten-free diets in reducing adiposity gain,inflammation and insulin resistance. The data suggests that diet gluten exclusion should be tested as a new dietary approach to prevent the development ofobesity and metabolic disorders.© 2013 Elsevier Inc. All rights reserved.

Keywords: Gluten-free diet; Obesity; Inflammation; Insulin resistance; PPAR

1. Introduction

Gluten is a protein complex consisting of glutenins and prolamins,whichmaybepresent in several cereals, suchaswheat, ryeandbarley [1].

Although a gluten-free diet is a well-established treatment forcoeliac disease, nowadays gluten-free diets have been proposed to beused for the prevention and treatment of diseases such as rheumatoidarthritis [2], Type 1 diabetes mellitus [3–5], obesity and insulinresistance (IR) [6].

Obesity is associated with important comorbidities that compro-mise an individual's health in many countries around the world [7,8].In particular, the accumulation of visceral fat is the common link tometabolic syndrome, atherosclerosis and Type 2 diabetes mellitus [9–11]. Diet, as a part of lifestyle modification, is the primary strategy forthe prevention and treatment of obesity. For this reason, gluten-freediets have been used as an anti-obesity, anti- inflammatory and anti-diabetic strategy. However, well-controlled in vivo studies evaluatingthe benefice of such dietary approaches are rare in the literature.

The aim of this studywas to evaluate the effect of a gluten-free dieton body weight and adiposity gains, the inflammatory profile ofadipose tissue and glucose homeostasis using an experimental modelof diet-induced obesity.

2. Methods and materials

This project was approved by the Ethics Committee for Animal Experimentation atthe Federal University of Minas Gerais (protocols #222/08 and #161/2010).

Available online at www.sciencedirect.com

Journal of Nutritional Biochemistry 24 (2013) 1105–1111

☆ Funding sources: CAPES (www.capes.gov.br) and PRPq/UFMG (Pró-reitoria de pesquisa da UFMG).

☆☆ Conflict of interest: The authors declare that there are no conflicts ofinterest in regard to this study.

⁎ Corresponding author. Departamento de Bioquímica e Imunologia, ICB/UFMG. Belo Horizonte, CEP: 30161–970 MG, Brazil. Tel.: +55 3196061178;fax: +55 3134092614.

E-mail address: [email protected] (F.L.P. Soares).

0955-2863/$ - see front matter © 2013 Elsevier Inc. All rights reserved.http://dx.doi.org/10.1016/j.jnutbio.2012.08.009


Journal of Nutritional Biochemistry 2013; 24; 1105–11.

* food intake and lipid excretion were similar in both groups *


Journal of Nutritional Biochemistry 2013; 24; 1105–11.terça-feira, 13 de janeiro de 2015

Review

Does wheat make us fat and sick?q

Fred J.P.H. Brouns a,*, Vincent J. van Buul a, Peter R. Shewry baMaastricht University, Faculty of Health, Medicine and Life Sciences, Department of Human Biology, Health Food Innovation Management, P.O. Box 616,6200 MD Maastricht, The NetherlandsbRothamsted Research, Plant Biology and Crop Science, West Common, Harpenden, Hertfordshire AL5 2JQ, United Kingdom

a r t i c l e i n f o

Article history:Received 5 February 2013Received in revised form27 May 2013Accepted 3 June 2013

Keywords:Whole-wheatRisk-benefitGluten-free dietCeliac disease

a b s t r a c t

After earlier debates on the role of fat, high fructose corn syrup, and added sugar in the aetiology of obesity,it has recently been suggested that wheat consumption is involved. Suggestions have been made thatwheat consumption has adverse effects on health by mechanisms related to addiction and overeating. Wediscuss these arguments and conclude that they cannot be substantiated. Moreover, we conclude thatassigning the cause of obesity to one specific type of food or food component, rather than overconsumptionand inactive lifestyle in general, is not correct. In fact, foods containing whole-wheat, which have beenprepared in customary ways (such as baked or extruded), and eaten in recommended amounts, have beenassociated with significant reductions in risks for type 2 diabetes, heart disease, and a more favourable longterm weight management. Nevertheless, individuals that have a genetic predisposition for developingceliac disease, or who are sensitive or allergic to wheat proteins, will benefit from avoiding wheat and othercereals that contain proteins related to gluten, including primitive wheat species (einkorn, emmer, spelt)and varieties, rye and barley. It is therefore important for these individuals that the food industry shoulddevelop a much wider spectrum of foods, based on crops that do not contain proteins related to gluten,such as teff, amaranth, oat, quinoa, and chia. Based on the available evidence, we conclude that whole-wheat consumption cannot be linked to increased prevalence of obesity in the general population.

! 2013 The Authors. Published by Elsevier Ltd. All rights reserved.

1. Introduction

Wheat is the most widely cultivated cereal grain worldwide,being grown in temperate climates from Scandinavia in thenorth to Argentina in the south, including upland regions in thetropics. It is third among the cereals, behind maize and rice, intotal global production, which was 704 million tons in 2011. Thedemand for wheat for human consumption is also increasingglobally, including in countries which are climatically unsuitedfor wheat production, due to the adoption of western-stylediets. Wheat is relatively rich in micronutrients, includingminerals and B vitamins, and supplies up to 20% of the energyintake of the global population (Cummins and Roberts-Thomson,2009).

About 95% of the wheat that is grown and consumed globally isbread wheat (Triticum aestivum). Bread wheat is a relatively newspecies, having arisen in southeast Turkey about 9000 years ago(Feldman and Millet, 2001). It is hexaploid with three related ge-nomes (termed A, B and D) and probably arose by spontaneoushybridization between a cultivated form of tetraploid wheat (Tri-ticum turgidum) and a related wild grass species (goat grass, Aegi-lops tauschii). Most of the remaining 5% of the wheat crop istetraploid durum wheat (also called pasta wheat) (T. turgidum vardurum) which is more adapted to the dry Mediterranean climate.However, small amounts of “primitive” wheats are also grown,mainly for specialist health foods: einkorn (diploid Triticum mon-ococcum), emmer (tetraploid T. turgidum var dicoccon) and spelt(hexaploid T. aestivum var spelta). The latter essentially differs frombread wheat in that the hull is not removed by threshing; resultingin a higher fibre content when consumed as whole grain.

Although wheat is a young species, it is immensely diverse, withforms adapted to a wide range of local environments and selectedfor different end uses. Feldman et al. (1995) estimated that at least25,000 genetically distinct forms occur, but this is undoubtedly anunderestimate with previously unreported diversity beingdescribed in recent years in countries such as China. Determinationof the full genome sequence of bread wheat has been hindered bythemassive genome size (17 gigabases, which is 40 times the size of

Abbreviations: ATIs, amylase-trypsin inhibitors; CD, celiac disease; GI, glycemicindex; IBS, irritable bowel syndrome.q This is an open-access article distributed under the terms of the Creative

Commons Attribution License, which permits unrestricted use, distribution, andreproduction in any medium, provided the original author and source are credited.* Corresponding author. Tel.: þ31 (0) 433 88 14 66; fax: þ31 (0) 433 67 09 76.

E-mail addresses: [email protected] (F.J.P.H. Brouns),[email protected] (V.J. van Buul), [email protected](P.R. Shewry).

Contents lists available at SciVerse ScienceDirect

Journal of Cereal Science

journal homepage: www.elsevier .com/locate/ jcs

0733-5210/$ e see front matter ! 2013 The Authors. Published by Elsevier Ltd. All rights reserved.http://dx.doi.org/10.1016/j.jcs.2013.06.002

Journal of Cereal Science 58 (2013) 209e215


Weight Changes during 2 Years According to Diet Group


Metabolic Effects of WeightLoss on a Very-Low-CarbohydrateDiet Compared With an IsocaloricHigh-Carbohydrate Diet in Abdominally Obese Subjects

Jeannie Tay, BNUTRDIET (HONS),*† Grant D. Brinkworth, PHD,* Manny Noakes, PHD,*Jennifer Keogh, MSC,* Peter M. Clifton, PHD*

Adelaide, Australia

Objectives This study was designed to compare the effects of an energy-reduced, isocaloric very-low-carbohydrate, high-fat(VLCHF) diet and a high-carbohydrate, low-fat (HCLF) diet on weight loss and cardiovascular disease (CVD) riskoutcomes.

Background Despite the popularity of the VLCHF diet, no studies have compared the chronic effects of weight loss and meta-bolic change to a conventional HCLF diet under isocaloric conditions.

Methods A total of 88 abdominally obese adults were randomly assigned to either an energy-restricted (!6 to 7 MJ, 30%deficit), planned isocaloric VLCHF or HCLF diet for 24 weeks in an outpatient clinical trial. Body weight, bloodpressure, fasting glucose, lipids, insulin, apolipoprotein B (apoB), and C-reactive protein (CRP) were measured atweeks 0 and 24.

Results Weight loss was similar in both groups (VLCHF "11.9 # 6.3 kg, HCLF "10.1 # 5.7 kg; p $ 0.17). Blood pres-sure, CRP, fasting glucose, and insulin reduced similarly with weight loss in both diets. The VLCHF diet producedgreater decreases in triacylglycerols (VLCHF "0.64 # 0.62 mmol/l, HCLF "0.35 # 0.49 mmol/l; p $ 0.01) andincreases in high-density lipoprotein cholesterol (HDL-C) (VLCHF 0.25 # 0.28 mmol/l, HCLF 0.08 # 0.17mmol/l; p $ 0.002). Low-density lipoprotein cholesterol (LDL-C) decreased in the HCLF diet but remained un-changed in the VLCHF diet (VLCHF 0.06 # 0.58 mmol/l, HCLF "0.46 # 0.71 mmol/l; p % 0.001). However, ahigh degree of individual variability for the LDL response in the VLCHF diet was observed, with 24% of individu-als reporting an increase of at least 10%. The apoB levels remained unchanged in both diet groups.

Conclusions Under isocaloric conditions, VLCHF and HCLF diets result in similar weight loss. Overall, although both diets hadsimilar improvements for a number of metabolic risk markers, an HCLF diet had more favorable effects on theblood lipid profile. This suggests that the potential long-term effects of the VLCHF diet for CVD risk remain a con-cern and that blood lipid levels should be monitored. (Long-term health effects of high and low carbohydrate,weight loss diets in obese subjects with the metabolic syndrome; http://www.anzctr.org.au; ACTR No.12606000203550). (J Am Coll Cardiol 2008;51:59–67) © 2008 by the American College of CardiologyFoundation

Current dietary recommendations for weight managementand obesity treatment advocate the consumption of ahigh-carbohydrate, low-fat (HCLF), moderate energy-restricted diet (1,2). However, there has been a resurgence

in public interest in and use of a very-low-carbohydrate,high-fat (VLCHF) diet fueled by the epidemic of obesityand type 2 diabetes (3), and several recent randomizedcontrolled trials have demonstrated greater weight lossfollowing the consumption of an VLCHF diet comparedwith a HCLF diet up to 6 months (4–7). However, thesestudies have been largely limited by high attrition rates, poordietary compliance, and limited dietary assessment. Morerecently, Gardner et al. (8) published a study that used moreintensive interventional strategies to achieve better dietarycompliance and higher subject retention and demonstratedgreater weight loss in overweight/obese women following an

From the *Commonwealth Scientific and Industrial Research Organisation–Human Nutrition, Adelaide, Australia; and the †Department of Nutrition andDietetics, Flinders University, Adelaide, Australia. This study was supported byproject grants from the National Heart Foundation of Australia and the NationalHealth and Medical Research Council of Australia. For full author contributionand disclosure information, please see the end of this article.

Manuscript received April 11, 2007; revised manuscript received July 27, 2007,accepted July 30, 2007.

Journal of the American College of Cardiology Vol. 51, No. 1, 2008© 2008 by the American College of Cardiology Foundation ISSN 0735-1097/08/$34.00Published by Elsevier Inc. doi:10.1016/j.jacc.2007.08.050

J Am Coll Cardiol 2008;51:59–67.

22.2 ! 71.6 g/day in the HCLF diet with energy restric-tion. Plasma ketone concentrations were not different be-tween the groups at baseline. There was a significant time bydiet interaction for ketone bodies (p " 0.001) such thatlevels had increased more in the VLCHF diet comparedwith the HCLF diet by week 8 (Fig. 2). Ketone concentra-tions declined in the VLCHF diet during the subsequent 16weeks but remained 2-fold higher compared to the HCLFdiet at week 24, indicating compliance to a very-low-carbohydrate intake on the VLCHF diet. At week 24,carbohydrate intake negatively correlated with ketone con-centration in the VLCHF diet (r # $0.37, p # 0.01), butnot the HCLF diet (r # $0.17, p # 0.29). At baseline,physical activity levels were similar in both groups (p #0.55) and did not change in either group during theintervention (p # 0.83).Weight loss. Over the 24 weeks, there were substantialreductions in body weight in both groups (p " 0.001), withno significant difference between the diets, expressed either inabsolute terms (VLCHF $11.9 ! 6.3 kg, HCLF $10.1 !5.7 kg; p # 0.17) (Fig. 3) or as percentage weight loss(VLCHF $12.3 ! 5.5%, HCLF $10.5 ! 5.5%; p # 0.14).There was no effect of gender. The ITT with either baselinevalues carried forward or the last follow-up visit carriedforward for those who did not complete the study also showedno difference in weight loss between the diets (p ! 0.23).Furthermore, there were no differences between the diets forthe proportion of subjects that exhibited %5% weight loss(VLCHF 41 of 45, HCLF 35 of 43; chi-square # 1.76; p #0.18) and 10% weight loss (VLCHF 30 of 45, HCLF 23 of43; chi-square # 1.594; p # 0.21). Subjects in the highest

tertile of carbohydrate intake at baseline (%214 g/day) didnot experience greater weight loss on the VLCHF dietcompared with the HCLF diet (p # 0.10, time by dietinteraction). At week 24, weight loss correlated with ketoneconcentration in the VLCHF diet (r # 0.45, p # 0.002),but not in the HCLF diet (r # 0.20, p # 0.20).Lipids and apoB. There was a significant effect of diet ontotal and LDL-C (p " 0.005, time by diet interaction)whereby these parameters decreased in the HCLF diet (p "0.001) but did not change in the VLCHF diet (p ! 0.52)(Table 3). Subjects in the highest tertile according tobaseline LDL-C (%4.11 mmol/l, n # 29) showed largerLDL-C reductions in the HCLF diet compared with theVLCHF diet (VLCHF $0.23 ! 0.54 mmol/l, HCLF$0.76 ! 0.72 mmol/l; p # 0.03). A greater proportion ofsubjects on the VLCHF diet compared with the HCLF dietexperienced an increase in LDL-C of at least 5% (VLCHF36% [16 of 45]; HCLF 12% [5 of 42]; chi-square # 6.64,p # 0.01) and 10% (VLCHF 24% [11 of 45]; HCLF 10%[4 of 42]; chi-square # 3.39, p # 0.06). The LDLdecreased in 58% (26 of 45) and 79% (33 of 42) of subjectson the VLCHF and HCLF diets, respectively (chi-square #4.30, p # 0.04). For LDL-C, a significant effect of genderwas also observed (p # 0.04 time & diet & genderinteraction), such that LDL-C decreased in both genderson the HCLF diet (men $0.57 ! 0.97 mmol/l, women$0.39 ! 0.51 mmol/l; p # 0.57) but increased in men anddecreased in women on the VLCHF diet (men 0.21 ! 0.62mmol/l, women $0.18 ! 0.52 mmol/l; p # 0.03). Com-pared to baseline, apoB concentrations were reduced by 1%in the VLCHF diet and 4.9% in the HCLF diet, but thisdid not reach statistical significance, and there was nodifference between the diets (p # 0.52) (Table 3).

Figure 2 Plasma Ketone ConcentrationsBefore and After Intervention

Ketone concentration at baseline and after 8 and 24 weeks of energy restric-tion with an VLCHF diet (n # 45) or an HCLF diet (n # 43). *Significant time bydiet interaction between the groups (P"0.001) by repeated measures analysisof variance. †p " 0.001, ‡p # 0.01 significantly greater than HCLF by post-hoc comparisons at each time point with Bonferonni adjustment for 3 compari-sons. Abbreviations as in Figure 1.

Figure 3 Body Weight Before and After Intervention

Body weight at baseline and after 24 weeks of energy restriction consumptionof an VLCHF diet (n # 45) or an HCLF diet (n # 43). Both diets significantlydifferent (p " 0.001) from baseline (time effect). There was no significant timeby diet interaction (p % 0.05) over 24 weeks by repeated-measures analysis ofvariance. Abbreviations as in Figure 1.

63JACC Vol. 51, No. 1, 2008 Tay et al.January 1/8, 2008:59–67 Metabolic Effects of VLCHF Diets


Mean Change in Body Weight from Baseline to 2 Years According to Dietary Macronutrient Content

PTN: 25 x 15% LIP: 40 x 20% HC: 65 x 35%


Mean Change in Waist Circumference from Baseline to 2 Years According to Dietary Macronutrient Content

PTN: 25 x 15% LIP: 40 x 20% HC: 65 x 35%


ORIGINAL CONTRIBUTION

Comparison of the Atkins, Ornish, WeightWatchers, and Zone Diets for Weight Lossand Heart Disease Risk ReductionA Randomized TrialMichael L. Dansinger, MDJoi Augustin Gleason, MS, RDJohn L. Griffith, PhDHarry P. Selker, MD, MSPHErnst J. Schaefer, MD

POPULAR DIETS HAVE BECOME IN-creasingly prevalent and con-troversial.1 More than 1000 dietbooks are now available,2 withmany popular ones departing substan-tially from mainstream medical ad-vice.3 Cover stories for major newsmagazines, televised debates, and cau-tionary statements by prominent medi-cal authorities4,5 have fueled public in-terest and concern regarding theeffectiveness and safety of such diets.6-8

Although some popular diets arebased on long-standing medical ad-vice and recommend restriction of por-tion sizes and calories (eg, WeightWatchers),9 a broad spectrum of alter-natives has evolved. Some plans mini-mize carbohydrate intake without fatrestriction (eg, Atkins diet),10 manymodulate macronutrient balance andglycemic load (eg, Zone diet),11 and oth-ers restrict fat (eg, Ornish diet).12 Giventhe growing obesity epidemic,13 manypatients and clinicians are interested inusing popular diets as individualizedeating strategies for disease preven-tion.14 Unfortunately, data regarding therelative benefits, risks, effectiveness, and

For editorial comment see p 96.

Author Affiliations: Division of Endocrinology, Dia-betes, and Metabol ism (Drs Dansinger andSchaefer), and Institute for Clinical Research andHealth Policy Studies (Drs Griffith and Selker), Tufts-New England Medical Center; and Lipid MetabolismLaboratory, Jean Mayer US Department of Agricul-ture Human Nutr i t ion Research Center on

Aging, Tufts University (Dr Schaefer and Ms Glea-son), Boston, Mass.Corresponding Author: Michael L. Dansinger, MD,Atherosclerosis Research Laboratory, Tufts-New En-gland Medical Center, Box 216, Boston Dispensary 342,750 Washington St, Boston, MA 02111 ([email protected]).

Context The scarcity of data addressing the health effects of popular diets is an im-portant public health concern, especially since patients and physicians are interestedin using popular diets as individualized eating strategies for disease prevention.

Objective To assess adherence rates and the effectiveness of 4 popular diets (At-kins, Zone, Weight Watchers, and Ornish) for weight loss and cardiac risk factor re-duction.

Design, Setting, and Participants A single-center randomized trial at an aca-demic medical center in Boston, Mass, of overweight or obese (body mass index: mean,35; range, 27-42) adults aged 22 to 72 years with known hypertension, dyslipidemia,or fasting hyperglycemia. Participants were enrolled starting July 18, 2000, and ran-domized to 4 popular diet groups until January 24, 2002.

Intervention A total of 160 participants were randomly assigned to either Atkins(carbohydrate restriction, n=40), Zone (macronutrient balance, n=40), Weight Watch-ers (calorie restriction, n=40), or Ornish (fat restriction, n=40) diet groups. After 2 monthsof maximum effort, participants selected their own levels of dietary adherence.

Main Outcome Measures One-year changes in baseline weight and cardiac riskfactors, and self-selected dietary adherence rates per self-report.

Results Assuming no change from baseline for participants who discontinued the study,mean (SD) weight loss at 1 year was 2.1 (4.8) kg for Atkins (21 [53%] of 40 participantscompleted, P=.009), 3.2 (6.0) kg for Zone (26 [65%] of 40 completed, P=.002), 3.0(4.9) kg for Weight Watchers (26 [65%] of 40 completed, P! .001), and 3.3 (7.3) kg forOrnish (20 [50%] of 40 completed, P=.007). Greater effects were observed in study com-pleters. Each diet significantly reduced the low-density lipoprotein/high-density lipopro-tein (HDL) cholesterol ratio by approximately 10% (all P!.05), with no significant effectson blood pressure or glucose at 1 year. Amount of weight loss was associated with self-reported dietary adherence level (r=0.60; P!.001) but not with diet type (r=0.07; P=.40).For each diet, decreasing levels of total/HDL cholesterol, C-reactive protein, and insulinwere significantly associated with weight loss (mean r=0.36, 0.37, and 0.39, respec-tively) with no significant difference between diets (P=.48, P=.57, P=.31, respectively).

Conclusions Each popular diet modestly reduced body weight and several cardiacrisk factors at 1 year. Overall dietary adherence rates were low, although increasedadherence was associated with greater weight loss and cardiac risk factor reductionsfor each diet group.JAMA. 2005;293:43-53 www.jama.com

©2005 American Medical Association. All rights reserved. (Reprinted) JAMA, January 5, 2005—Vol 293, No. 1 43

Downloaded From: http://jama.jamanetwork.com/ on 03/23/2014

JAMA. 2005;293:43-53.

One way to improve dietary adher-ence rates in clinical practice may be touse a broad spectrum of diet options, tobetter match individual patient food pref-erences, lifestyles, andcardiovascular riskprofiles. Participants in our study werenot allowed to choose their dietary as-signment; however, we suspect adher-ence rates and clinical improvementswould have been better if participantshad been able to freely select from the 4diet options. Our findings challenge theconcept that 1 type of diet is best for ev-erybody and that alternative diets can bedisregarded. Likewise, our findings donot support the notion that very low car-bohydrate diets are better than stan-dard diets, despite recent evidence to thecontrary.17,22,23,25

Our results support a growing bodyof research suggesting that carbohy-drate restriction and saturated fat re-striction have different effects on car-diovascular r i sk prof i les . Lowcarbohydrate diets consistently in-crease HDL cholesterol,17,20 and low–saturated fat diets consistently de-crease LDL cholesterol levels.34 Lowcarbohydrate diets have typically beenmore effective for short-term reduc-tion of serum triglycerides, glucose,

and/or insulin.17,19,22,23,35,36 These find-ings may suggest to some clinicians thatthe degree to which a patient exhibitsfeatures of the metabolic syndrome

might guide the degree of carbohy-drate restriction to recommend. In thelong run, however, sustained adher-ence to a diet rather than diet type was

Figure 3. One-Year Changes in Body Weight as a Function of Diet Group and DietaryAdherence Level for All Study Participants

15

–25

r = 0.07, P = .40 r = –0.60, P

Dieta Cetogênica e Emagrecimento: Vias Metabólicas Envolvidas


Low-Carbohydrate Diets and All-Cause Mortality: ASystematic Review and Meta-Analysis of ObservationalStudiesHiroshi Noto1,2*, Atsushi Goto1,2, Tetsuro Tsujimoto1,2, Mitsuhiko Noda1,2

1Department of Diabetes and Metabolic Medicine, Center Hospital, National Center for Global Health and Medicine, Tokyo, Japan, 2Department of Diabetes Research,

Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan

Abstract

Objective: Low-carbohydrate diets and their combination with high-protein diets have been gaining widespread popularityto control weight. In addition to weight loss, they may have favorable short-term effects on the risk factors of cardiovasculardisease (CVD). Our objective was to elucidate their long-term effects on mortality and CVD incidence.

Data sources: MEDLINE, EMBASE, ISI Web of Science, Cochrane Library, and ClinicalTrials.gov for relevant articles publishedas of September 2012. Cohort studies of at least one year’s follow-up period were included.

Review methods: Identified articles were systematically reviewed and those with pertinent data were selected for meta-analysis. Pooled risk ratios (RRs) with 95% confidence intervals (CIs) for all-cause mortality, CVD mortality and CVD incidencewere calculated using the random-effects model with inverse-variance weighting.

Results: We included 17 studies for a systematic review, followed by a meta-analysis using pertinent data. Of the 272,216people in 4 cohort studies using the low-carbohydrate score, 15,981 (5.9%) cases of death from all-cause were reported. Therisk of all-cause mortality among those with high low-carbohydrate score was significantly elevated: the pooled RR (95% CI)was 1.31 (1.07–1.59). A total of 3,214 (1.3%) cases of CVD death among 249,272 subjects in 3 cohort studies and 5,081 (2.3%)incident CVD cases among 220,691 people in different 4 cohort studies were reported. The risks of CVD mortality andincidence were not statistically increased: the pooled RRs (95% CIs) were 1.10 (0.98–1.24) and 0.98 (0.78–1.24), respectively.Analyses using low-carbohydrate/high-protein score yielded similar results.

Conclusion: Low-carbohydrate diets were associated with a significantly higher risk of all-cause mortality and they were notsignificantly associated with a risk of CVD mortality and incidence. However, this analysis is based on limited observationalstudies and large-scale trials on the complex interactions between low-carbohydrate diets and long-term outcomes areneeded.

Citation: Noto H, Goto A, Tsujimoto T, Noda M (2013) Low-Carbohydrate Diets and All-Cause Mortality: A Systematic Review and Meta-Analysis of ObservationalStudies. PLoS ONE 8(1): e55030. doi:10.1371/journal.pone.0055030

Editor: Lamberto Manzoli, University of Chieti, Italy

Received November 7, 2012; Accepted December 18, 2012; Published January 25, 2013

Copyright: ! 2013 Noto et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permitsunrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: This study was supported by a Health Sciences Research Grant (Comprehensive Research on Diabetes/Cardiovascular and Life-Style Related DiseasesH22-019) from the Ministry of Health, Labour and Welfare of Japan. The funders had no role in study design, data collection and analysis, decision to publish, orpreparation of the manuscript.

Competing Interests: The authors have declared that no competing interests exist.

* E-mail: [email protected]

Introduction

A growing body of evidence has suggested that low-carbohy-drate diets and their combination with high-protein diets areeffective in weight loss. [1–3] In addition, they reportedlyameliorate the risk factors of cardiovascular disease (CVD) inthe short term, [4–6] which would decrease incident CVD andmortality. However, recent cohort studies did not support thishypothesis [7–12] and their long-term health benefit and riskremain controversial. In fact, low-carbohydrate diets tend to resultin reduced intake of fiber and fruits, and increased intake ofprotein from animal sources, cholesterol and saturated fat, all ofwhich are risk factors for mortality and CVD. [13,14].

In light of the worldwide obesity epidemic and the widespreadpopularity of low-carbohydrate diets, explorations of their long-term health outcome are of clinical importance for the control ofweight. Moreover, they are crucial in the areas of public health,since a modest increase in the risk of morbidity and mortality [15]translates into a substantial social burden. These circumstancesprompted us to investigate, with greater precision, the effects oflow-carbohydrate diets on mortality and CVD incidence byscrutinizing pertinent original reports and combining their data inan attempt to obtain meaningful clues for the evaluation of benefitand harm associated with dietary modification.

PLOS ONE | www.plosone.org 1 January 2013 | Volume 8 | Issue 1 | e55030

consequences of low-carbohydrate diets with respect to kidneydisease, osteoporosis, and mental condition. The biology thatunderlies the positive correlation between low-carbohydrate dietsand all-cause death is not fully explained. Further studies to clarifythe mechanism are eagerly awaited.Given the facts that low-carbohydrate diets are likely unsafe and

that calorie restriction has been demonstrated to be effective inweight loss regardless of nutritional composition, [36] it would beprudent not to recommend low-carbohydrate diets for the timebeing. Further detailed studies to evaluate the effect of proteinsource are urgently needed.

LimitationsAlthough the quality of the included studies might not be an

issue, our analysis should be interpreted in the context of thefollowing limitations. The observational studies were scarce andmoderately heterogeneous, and thus a publication bias and aresidual confounding bias may have existed although we cannotassess these hypotheses. In the analysis of CVD mortality risk,there may not have been enough statistical power and therepresentativeness of the cohort may be poor since the data ofhealthcare professionals [7] dominated (Fig. 3A). Next, therelation may not necessarily be causal, particularly in theobservational studies [37] because of possible confounding factorsand biases that may not have been fully adjusted for, which mayhave rendered the results less valid. In our analysis, the adjustment

in each component study was adequate and fair. Confounding bytreatment indication [38] might bias the effect of diets. However,most of the target populations were free of chronic disease atbaseline and it is less likely that the dietary habits had beenmodulated according to their previous health status. A dose-response of relative risk was confirmed in few studies, which mightmake the results less plausible. Dietary patterns may vary over thecourse of follow-up but updating dietary information was not donein many studies and thus the magnitude of risk may have beendiluted as suggested by our subgroup analysis of the flow-upperiods and the supplementary analysis by Lagiou, et al. [9]Furthermore, it is difficult to distinguish the effects of individualnutritional component. For all these limitations, however,observational studies provide good available evidence regardingpotential benefit and harm, and the overall pooled estimates wererobust, the temporal sequence of the events was appropriate, andthe results among the included studies seemed consistent.Moreover, evidence has been accumulating to support thesepotential adverse outcomes. [39] With regards to external validity,it is also important to realize that the participants of the studiesmay not represent general populations most likely because themajority of the studies were done in Western countries andhealthcare professionals dominated. It remains unclear if thesediets exert a similar influence on the clinical outcome in diabeticpatients.

Figure 2. Adjusted risk ratios for all-cause mortality associated with low-carbohydrate diets. Analysis was done based on (A) the low-carbohydrate score and (B) the low-carbohydrate/high-protein score. Boxes, estimated risk ratios (RRs); bars, 95% confidence intervals (CIs).Diamonds, random-effects model RRs; width of diamonds; pooled CIs. The size of each box is proportional to the weight of each study in the meta-analysis. IV, inverse-variance.doi:10.1371/journal.pone.0055030.g002

Low-Carbohydrate Diets and Mortality

PLOS ONE | www.plosone.org 8 January 2013 | Volume 8 | Issue 1 | e55030

PLoS 2013; 8(1): e55030.terça-feira, 13 de janeiro de 2015

Pesquisa realizada na madrugada do dia 06.11.2014

Prescrição de Dieta Detox: Com que evidência mesmo?


E os termogênicos, hein?


Am J Clin Nutr. 1984;40:995-1000.

Termogênese induzida pela dieta

Gasto energético com atividade física

TMB

Indivíduo sedentário(1800 kcal/d)

Indivíduo fisicamente ativo(2200 kcal/d)

8% 17%

75%

8%

60%

32%


Nº 93, segunda-feira, 19 de maio de 2014 131ISSN 1677-7042

Este documento pode ser verificado no endereço eletrônico http://www.in.gov.br/autenticidade.html ,pelo código 00012014051900132

Documento assinado digitalmente conforme MP no- 2.200-2 de 24/08/2001, que institui aInfraestrutura de Chaves Públicas Brasileira - ICP-Brasil.

1

16. Os Contadores que pretendam atuar em auditoria desociedades supervisionadas pela SUSEP deverão ainda se submeter àprova específica na qual serão exigidos conhecimentos nas seguintesáreas:

(a) Legislação Profissional;(b) Normas Brasileiras de Contabilidade, Técnicas e Pro-

fissionais, editadas pelo Conselho Federal de Contabilidade;(c) Legislação e normas operacionais aplicáveis às socie-

dades supervisionadas pela SUSEP;(d) Conhecimentos de operações da área de sociedades su-

pervisionadas pela SUSEP;(e) Contabilidade de seguradoras, entidades abertas de pre-

vidência complementar, sociedades de capitalização e reseguradoreslocais; e

(f) Língua Portuguesa Aplicada.17. O CFC, por intermédio da Vice-presidência de Desen-

volvimento Profissional e Institucional deve providenciar a divul-gação em seu portal dos conteúdos programáticos das respectivasáreas que serão exigidos nas provas, com a antecedência mínima de60 (sessenta) dias em relação à data da aplicação das provas.

Aprovação e periodicidade do exame18. O candidato é aprovado se obtiver, no mínimo, 50%

(cinquenta por cento) dos pontos das questões objetivas e 50% (cin-quenta por cento) dos pontos das questões dissertativas previstos paracada prova.

19. O Exame deve ser aplicado pelo menos uma vez a cadaano, em dia, data e hora fixados no Edital pelo CFC, ou mais de umavez, por decisão do Plenário do CFC.

Certidão de aprovação20. Ocorrendo aprovação no Exame de Qualificação Técnica

para registro no CNAI do CFC, o CFC deve disponibilizar em suapágina na internet a certidão de aprovação no Exame, a partir da datade publicação do resultado no Diário Oficial da União, bem como suainclusão automática no CNAI.

Recursos21. O candidato inscrito no Exame de Qualificação Técnica

para registro no CNAI do CFC pode interpor recursos contra osgabaritos das provas e do resultado final publicado pelo CFC, semefeito suspensivo, dentro dos prazos e instâncias definidos previa-mente em edital.

Impedimentos: preparação de candidatos e participação22. O CFC e os CRCs, seus conselheiros efetivos e su-

plentes, seus funcionários, seus delegados e os integrantes da CAEnão poderão oferecer ou apoiar, a qualquer título, cursos preparatóriospara os candidatos ao Exame de Qualificação Técnica para registro noCNAI do CFC ou deles participar, sob qualquer título.

23. Os membros efetivos da CAE não poderão se submeterao Exame de Qualificação Técnica de que trata esta Norma, noperíodo em que estiverem nessa condição.

24. O descumprimento do disposto no item antecedente secaracteriza infração de natureza ética, sujeitando-se o infrator às pe-nalidades previstas no Código de Ética Profissional do Contador.

Divulgação25. O CFC deve desenvolver campanha no sentido de es-

clarecer e divulgar o Exame de Qualificação Técnica para registro noCNAI do CFC, os CRCs devem reforçar essa divulgação nas suasjurisdições.

Banco de questões26. A CAE pode solicitar, por intermédio da Vice-presi-

dência de Desenvolvimento Profissional e Institucional, a entidadesou a instituições de renomado reconhecimento técnico, sugestões dequestões para a composição do banco de questões a ser utilizado paraa elaboração das provas.

Disposições finais27. Ao CFC cabe adotar as providências necessárias ao aten-

dimento do disposto na presente Norma, competindo ao seu Plenáriointerpretá-la quando se fizer necessário.

Vi g ê n c i a28. Esta Norma entra em vigor na data de sua publicação e

revoga a Resolução CFC n.º 1.109/07, publicada no D.O.U., Seção I,de 6/12/07.

JOSÉ MARTONIO ALVES COELHOPresidente do Conselho

CONSELHO FEDERAL DE NUTRICIONISTASRESOLUÇÃO Nº 541, DE 14 DE MAIO DE 2014

Altera o Código de Ética do Nutricionista,aprovado pela Resolução CFN nº 334, de2004, e dá outras providências.

O Presidente do Conselho Federal de Nutricionistas (CFN),no uso das atribuições que lhe são conferidas pela Lei n° 6.583, de 20de outubro de 1978, regulamentada pelo Decreto n° 84.444, de 30 dejaneiro de 1980, e no Regimento Interno aprovado pela ResoluçãoCFN nº 320, de 2 de dezembro de 2003, ouvidos os ConselhosRegionais de Nutricionistas (CRN), e, tendo em vista o que foideliberado na 262ª Reunião Plenária, Ordinária, do CFN, esta rea-lizada nos dias 22, 23 e 24 de fevereiro de 2014, resolve:

Art. 1º. Os artigos 6°, 7°, 15, 16, 19 e 21 do Código de Éticado Nutricionista, aprovado pela Resolução CFN nº 334, de 10 demaio de 2004, passam a vigorar com as seguintes redações: "Art. 6º.(...) I - realizar, unicamente em consulta presencial, a avaliação e odiagnóstico nutricional e a respectiva prescrição dietética do indi-víduo sob sua responsabilidade profissional; (...) VI - analisar comrigor técnico-científico qualquer tipo de prática ou pesquisa, ado-tando-a somente quando houver níveis consistentes de evidência cien-tífica ou quando integrada em protocolos implantados nos respectivosserviços; (...) Art. 7º. (...) XVII - realizar, por qualquer meio queconfigure atendimento não presencial, a avaliação e o diagnósticonutricional e a respectiva prescrição dietética do indivíduo sob sua

responsabilidade profissional; (...) Art. 15. (...) I - quando na funçãode docente, orientador ou supervisor de estágios, garantir ao es-tagiário supervisão frequente e sistemática, de forma ética e tec-nicamente compatível com a área do estágio, orientando sobre aimportância em observar os princípios e normas contidas neste Có-digo; (...) Art. 16. (...) I - quando na função de diretor de escolas deNutrição, coordenador de cursos ou coordenador/orientador de es-tágios aceitar, como campo de estágio instituições e empresas que nãodisponham no seu quadro de pessoal de nutricionista encarregado dasupervisão das atividades do estagiário ou quando não possa sergarantida a presença e acompanhamento de nutricionista docente; (...)Art. 19. (...) I - respeitar a legislação pertinente quando realizarpesquisa envolvendo seres humanos ou animais; (...) Art. 21. Re-lativamente à publicidade, é dever do nutricionista, por ocasião deentrevistas, comunicações, publicações de artigos e informações aopúblico sobre alimentação, nutrição e saúde, preservar o decoro pro-fissional, basear suas informações em conteúdo referendado em pes-quisas realizadas com rigor técnico-científico, e assumir inteira res-ponsabilidade pelas informações prestadas. Art. 2º. O art. 7° do Có-digo de Ética do Nutricionista, aprovado pela Resolução CFN nº 334,de 10 de maio de 2004, passa a vigorar acrescido dos seguintesparágrafos: § 1º. Para fins do inciso XVII deste artigo excetua-se omonitoramento do paciente/cliente que esteja temporariamente im-possibilitado para a realização da consulta presencial. § 2º. Com-preende-se: a) por consulta, a assistência em ambulatório, consultórioe em domicílio; b) por diagnóstico nutricional, o diagnóstico ela-borado a partir de dados clínicos, bioquímicos, antropométricos edietéticos; e c) prescrição dietética, a prescrição elaborada com basenas diretrizes estabelecidas no diagnóstico nutricional. Art. 3º. O art.22 do Código de Ética do Nutricionista, aprovado pela ResoluçãoCFN nº 334, de 10 de maio de 2004, passa a vigorar acrescido doseguinte parágrafo único: Parágrafo único. Para fins do inciso IIIdeste artigo, quando da orientação ou prescrição dietética, havendonecessidade de mencionar marcas, o nutricionista deverá indicar vá-rias alternativas oferecidas pelo mercado. Art. 4º. Revogam-se o pa-rágrafo único do art. 7° e o parágrafo único do art. 16 do Código deÉtica do Nutricionista, aprovado pela Resolução CFN nº 334, de 10de maio de 2004, alterada pela Resolução CFN nº 399, de 26 defevereiro de 2007. Art. 5º. Esta Resolução entra em vigor na data desua publicação.

ÉLIDO BONOMO

CONSELHO FEDERAL DE ODONTOLOGIARETIFICAÇÃO

No Diário Oficial da União, de 7 de outubro de 2004, Seção1, pág. 430, na Resolução CFO-59/2004, onde se lê no artigo 10: "§4º...", leia-se: "§ 3º.." e "§ 5º...", leia-se: "§ 4º.".

"Art. 6o. (...) VI - analisar com rigor técnico-científico qualquer tipo de prática ou pesquisa, adotando-a somente quando houver níveis consistentes de evidência científica ou quando integrada em protocolos implantados nos respectivos serviços; (...)


2013 AHA/ACC/TOS Guideline for theManagement of Overweight and Obesity in AdultsqA Report of the American College of Cardiology/American Heart AssociationTask Force on Practice Guidelines and The Obesity Society

Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation,American Pharmacists Association, American Society for Nutrition, American Society for Parenteraland Enteral Nutrition, American Society for Preventive Cardiology, American Society of Hypertension,Association of Black Cardiologists, National Lipid Association, Preventive CardiovascularNurses Association, The Endocrine Society, andWomenHeart: The National Coalition for Women With Heart Disease

Expert PanelMembers

Michael D. Jensen, MD, Co-ChairDonna H. Ryan, MD, Co-Chair

Caroline M. Apovian, MD, FACPJamy D. Ard, MDAnthony G. Comuzzie, PHDKaren A. Donato, SM*Frank B. Hu, MD, PHD, FAHAVan S. Hubbard, MD, PHD*John M. Jakicic, PHDRobert F. Kushner, MD

Catherine M. Loria, PHD, FAHA*Barbara E. Millen, DRPH, RDCathy A. Nonas, MS, RDF. Xavier Pi-Sunyer, MD, MPHJune Stevens, PHDVictor J. Stevens, PHDThomas A. Wadden, PHDBruce M. Wolfe, MDSusan Z. Yanovski, MD*

*Ex-Officio Members.

MethodologyMembers

Harmon S. Jordan, SCDKarima A. Kendall, PHDLinda J. LuxRoycelynn Mentor-Marcel, PHD, MPH

Laura C. Morgan, MAMichael G. Trisolini, PHD, MBAJanusz Wnek, PHD

ACC/AHA TaskForce Members

Jeffrey L. Anderson, MD, FACC, FAHA, ChairJonathan L. Halperin, MD, FACC, FAHA,

Chair-Elect

Nancy M. Albert, PHD, CCNS, CCRN, FAHABiykem Bozkurt, MD, PHD, FACC, FAHARalph G. Brindis, MD, MPH, MACCLesley H. Curtis, PHD, FAHA

David DeMets, PHDJudith S. Hochman, MD, FACC, FAHARichard J. Kovacs, MD, FACC, FAHAE. Magnus Ohman, MD, FACCSusan J. Pressler, PHD, RN, FAAN, FAHAFrank W. Sellke, MD, FACC, FAHAWin-Kuang Shen, MD, FACC, FAHA

Subcommittee onPreventionGuidelines

Sidney C. Smith, JR, MD, FACC, FAHA, Chair Gordon F. Tomaselli, MD, FACC, FAHA, Co-Chair

qCirculation is published on behalf of the American Heart Association, Inc., byWolters Kluwer; Obesity is published on behalf of The Obesity Society by JohnWiley and Sons Inc.; The Journal of the American College of Cardiology is publishedon behalf of the American College of Cardiology Foundation by Elsevier Inc. This isan open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDervis License, which permits use, distribution, and reproductionin any medium, provided that the Contribution is properly cited, the use isnoncommercial, and no modifications or adaptations are made.This document was approved by the American College of Cardiology Board of

Trustees, the American Heart Association Science Advisory and CoordinatingCommittee, and The Obesity Society Board of Trustees in November 2013. TheAcademy of Nutrition and Dietetics affirms the value of this guideline.

The American College of Cardiology requests that this document be cited asfollows: Jensen MD, Ryan DH, Apovian CM, Ard JD, Comuzzie AG, Donato KA,Hu FB, Hubbard VS, Jakicic JM, Kushner RF, Loria CM, Millen BE, Nonas CA,Pi-Sunyer FX, Stevens J, Stevens VJ, Wadden TA, Wolfe BM, Yanovski SZ. 2013AHA/ACC/TOS guideline for the management of overweight and obesity in adults:a report of the American College of Cardiology/American Heart Association Task Forceon PracticeGuidelines and TheObesity Society. J AmCollCardiol 2014;63:2985–3023.This article is copublished in Circulation and Obesity.Copies: This document is available on theWorldWideWeb sites of the American

College of Cardiology (http://www.cardiosource.org) and the American HeartAssociation (my.americanheart.org). For copies of this document, please contact theElsevier Inc. Reprint Department, fax (212) 462-1935, e-mail [email protected].

Journal of the American College of Cardiology! 2014 The Expert Panel MembersPublished by Elsevier Inc.

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overweight and obese patients. The CQs answered byevidence-based recommendations summarize currentliterature on the risks of overweight and obesity and thebenefits of weight loss. They also summarize knowledge onthe best diets for weight loss, the efficacy and effectivenessof comprehensive lifestyle interventions on weight loss andweight loss maintenance, and the benefits and risks ofbariatric surgery. This information will help PCPs decidewho should be recommended for weight loss and whathealth improvements can be expected. The Expert Paneldid not choose a CQ that dealt with various aspects ofpharmacotherapy for a comprehensive evidence assess-ment, because at the time the CQs were chosen there wasonly one approved medication (orlistat) for weight loss.However, CQ1 includes some ESs on the efficacy oforlistat because the effect of pharmacotherapy on weightloss was included in its evidence review.

2.2. Chronic Disease Management Model forPrimary Care of Patients With Overweight andObesitydTreatment Algorithm

The Expert Panel provides a treatment algorithm,Chronic Disease Management Model for Primary Careof Patients With Overweight and Obesity (Figure), toguide PCPs in the evaluation, prevention, and manage-ment of excess body weight in their patients. Thealgorithm incorporates, wherever possible, the recom-mendations derived from the 5 CQs that yielded ESs andrecommendations. However, because the 5 CQs thatwere considered did not cover the entire scope of eval-uation, prevention, and management of overweight/obesity, the panelists provided advice based on otherguidelines and expert opinion to give providers a morecomprehensive approach to their patients with weight-related issues.

Table 4. Summary of Recommendations for Obesity

RecommendationsNHLBIGrade

NHLBIES ACC/AHA COR ACC/AHA LOE

Identifying Patients Who Need to Lose Weight (BMI and Waist Circumference)

1a. Measure height and weight and calculate BMI at annual visits or more frequently. E (Expert Opinion) CQ2 I C

1b. Use the current cutpoints for overweight (BMI 25.0–29.9 kg/m2) and obesity(BMI !30 kg/m2) to identify adults who may be at elevated risk ofCVD and the current cutpoints for obesity (BMI !30 kg/m2) to identify adults whomay be at elevated risk of mortality from all causes.

A (Strong) CQ2 I B

1c. Advise overweight and obese adults that the greater the BMI, the greater therisk of CVD, type 2 diabetes, and all-cause mortality.

A (Strong) CQ2 I B

1d. Measure waist circumference at annual visits or more frequently inoverweight and obese adults.Advise adults that the greater the waist circumference, the greater the risk of CVD,type 2 diabetes, and all-cause mortality. The cutpoints currently in commonuse (from either NIH/NHLBI or WHO/IDF) may continue to be used to identifypatients who may be at increased risk until further evidence becomes available.

E (Expert Opinion) CQ2 IIa B

Matching Treatment Benefits With Risk Profiles (Reduction in Body Weight Effect on Risk Factors for CVD, Events, Morbidity and Mortality)

2. Counsel overweight and obese adults with cardiovascular risk factors (high BP,hyperlipidemia, and hyperglycemia) that lifestyle changes that produce even modest,sustained weight loss of 3%–5% produce clinically meaningful health benefits, andgreater weight losses produce greater benefits.a. Sustained weight loss of 3%–5% is likely to result in clinically meaningful

reductions in triglycerides, blood glucose, hemoglobin A1c, and the risk ofdeveloping type 2 diabetes;

b. Greater amounts of weight loss will reduce BP, improve LDL–C and HDL–C, andreduce the need for medications to control BP, blood glucose, and lipids as wellas further reduce triglycerides and blood glucose.

A (Strong) CQ1 I A

Diets for Weight Loss (Dietary Strategies for Weight Loss)

3a. Prescribe a diet to achieve reduced calorie intake for obese or overweight individualswho would benefit from weight loss, as part of a comprehensive lifestyle intervention.Any one of the following methods can be used to reduce food and calorie intake:a. Prescribe 1,200–1,500 kcal/d for women and 1,500–1,800 kcal/d for men

(kilocalorie levels are usually adjusted for the individual’s body weight);b. Prescribe a 500-kcal/d or 750-kcal/d energy deficit; orc. Prescribe one of the evidence-based diets that restricts certain food types (such

as high-carbohydrate foods, low-fiber foods, or high-fat foods) in order to createan energy deficit by reduced food intake.

A (Strong) CQ3 I A

3b. Prescribe a calorie-restricted diet, for obese and overweight individuals who wouldbenefit from weight loss, based on the patient’s preferences and health status, andpreferably refer to a nutrition professional* for counseling. A variety of dietaryapproaches can produce weight loss in overweight and obese adults, as presented inCQ3, ES2.

A (Strong) CQ3 I A

Continued on the next page

Jensen et al. JACC Vol. 63, No. 25, 20142013 AHA/ACC/TOS Guideline for Obesity July 1, 2014:2985–3023

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Obrigada!

Fonte da figura: https://www.facebook.com/NutricaoSemModismo?fref=tsterça-feira, 13 de janeiro de 2015
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