Este é um post popular. bassitos 99 Postado Junho 17, 2011 às 19:26 Este é um post popular. Compartilhar Postado Junho 17, 2011 às 19:26 (editado) ATENCAO, LEIA TUDO ANTES DE CRIAR UM POST CRITICANDO! Antes de virem falar que eu estou trollando aqui, eu venho em uma boa, criar um topico para criar uma discussao e abrir a mente das pessoas. Ah, antes que eu esqueca, meu teclado nao tem acentos nem cedilha, entao se acostumem, por favor Bom, ja participei dese forum por muito tempo, mas depois de um tempo parei. Muita gente se preucupa em comer dem 3 em 3 horas, isso ja foi comprovado que nao tem fundamento nenhum, nao vai influenciar em nada no seu metabolismo. Segunda coisa que eu gostaria de colocar em jogo aqui, voces acham que, realmente, precisa de uma dieta totalmente montada, voces comeram igual todos os dias? 1g de carboidrato é uma grama de carboidrato, nao importa, assim como 1g de proteina é uma 1 de proteina, e de gordura assim....ou seja, onde eu quro chegar nisso? Qual é a diferenca em termos de COMPOSICAO entre 50g de Carb, 50g de Prot e 20g de gordura proveniente de uma pizza ou de frango com brocolis e batata.....NENHUMA! Porém, existem MICRONUTRIENTES, que sao as vitaminas, minerais, etc e tals.....isso sim importa, porem voces acham mesmo que seu eu comendo essa pizza todo dia e continuar em deficit calorico, e atingir meus macronutrientes necessarios, eu nao emagrecerei? SIM, eu emagrecerei, por que? Porque o corpo utiliza a fonte mais baixa, ou seja, ela pega o seu frango ou o seu peperoni da pizza e quebra, quebra ate virar um aminoacido, e nao difere em nada de onde ele veio, seu corpo nao vai dizer: AH, ISSO É DE UMA PIZZA OU MCDONALDS, VOU TRANFORMAR EM GORDURA! NAO, por favor, nao, isso nao acontece.....Porem existem os micros, que possuem um papel fundamental na sua saude...ou seja, onde quero chegar? Muita gente espera uum dia da semana para comer chocolate, pizza e acaba criando um puta superavit calorico e, eventualmente, acaba estragando muito esforco.... Por que nao fazer isso TODO DIA, com moderacao? Quero chegar ao novo estilo de fazer uma dieta, proposto pelo topico.Que fique bem claro: IIFYM NAO é uma dieta, e sim uma forma de usar seus macros de uma forma correta, prazeirosa e saudávelEntao vamos comecar pelo comeco:Quantas calorias eu preciso e quais macronutrientes?Calorias:Harris-Benedict : HOMEM: BMR = 66 + [13.7 x peso (kg)] + [5 x altura (cm)] - [6.76 x idade (anos)] MULHER: BMR = 655 + [9.6 x peso (kg)] + [1.8 x altura (cm)] - [4.7 x idade (anos)]Mifflin-St Jeor: HOMEN: BMR = [9.99 x peso (kg)] + [6.25 x altura (cm)] - [4.92 x idade (anos)] + 5 MULHER: BMR = [9.99 x peso (kg)] + [6.25 x altura (cm)] - [4.92 x idade (anos)] -161Katch-McArdle: BMR = 370 + (21.6 x LBM) Onde LBM = Peso total em kg - Peso total kg x (Bodyfat % / 100)Exemplo: 100kg total x 100kg - (10% bf / 100) -> 100 - 100 x 0,1 -> 100 - 10 -> LBM = 90 kg Aconselhado é usar a ultima, se nao for possivel, use a segunda, pois a primeira tende a superestimar as necessidades caloricas, principalmente em individuos com sobre-peso Depois voce deverá multiplicar pelo fator de atividade: 1.2 = Sedentário (Pouco ou nenhum exercicio + desk job) 1.3-1.4 =Pouco ativo (Pouco ativo no dia-a-dia & exercicios lights 1-3 dias por semana) 1.5-1.6 = Moderadamente ativo (Moderadamente ativo no dia-a-dia & exercicios em intensidade moderada 3-5 dias por semana) 1.7-1.8 = Muito ativo (Estilo de vida que exige esforco bruto & Exercicio intenso ou reliza algum esporte 6-7 dias por semana) 1.9-2.0 = Extremamente ativo (Atividade de vida muito intensa ou esportes e trabalho fisico)Agora para calcular o seu OBJETIVO: Voce precisa ADICIONAR ou SUBTRAIR calorias para seu objetivo(perder peso ou ganhar). E ao inves de usar métodos genéricos, como 500kcal ao dia, voce deve usar PORCENTAGENS. Por que? Pois o deficit varia de pessoa para pesoa. Por exemplo: tirando 500kcal de uma dieta com 3000kcal vc tira 1/6 apenas, porem uma dieta de 1.500kcal voce tira 1/3, entao, o melhor protocolo seria: - Para GANHAR peso(Bulking): ADICIONE 10-20% do valor total que voce encontrou acima - Para PERDER peso(cutting): RETIRE 10-20% do valor total que voce encontrou acima Monitore seus resultados por 2 à 4 semanas, se seu peso nao mudar, voce achou sua manutencao calórica, entao voce deve aumentar. Se voce quer perder peso e nao perdeu, desca as calorias mais um pouco, e o mesmo para quem quer ganhar massa, se nao ganhar, suba as calorias um pouco Lembrando que esses valores, tanto para cutting ou bulking, sao valores para evitar ganho excessivo de gordura em bulking e perda excessiva de massa magra em cutting. Porém isso depende muito do individual, entao monitore como dito acima.Essas fórmulas sao precisas? As formulas sao apenas como ajuda, muitas pessoas acabam errando na hora de calcular seu nivel de atividade ou bodyfat, por isso pense muito bem antes de selecionar seu fator de atividade, pois muitos subestimam e acabam nao crescendo, enquanto outros comem demais O fator de atividade nao é relacionado apenas aos dias de academia, porém ao seu dia-a-diaCalculando macronutrientes:1. Proteina: Mesmo sendo em base de massa magra, pode-se ter uma base Proteina (gramas) = 1-1.5 x peso total (pounds) ou 2,2- 3,3 x peso total(kilogramas) Se voce é MUITO MAGRO ou um tem uma dieta BAIXA EM CALORIAS, entao voce precisa manter sempre alta as proteinas, mantendo sempre perto do valor maximo ou até mais Se voce é MUITO GORDO ou uma dieta ALTA EM CALORIAS, entao voce pode deixar nos valores mais baixos, ou até mesmo um pouco menos, como 2g/kg2. Gorduras: O corpo pode suportar pequenos periodos de baixa ingestao de gorduras, porém, gorduras sao extremamente necessarias para funcoes hormonais em um longo termo, para manter saude, sasiedade e sanidade. O ideal é manter 0.45g por massa magra em libras ou 1g por massa magra em kilogramas Se voce possui um gasto calorico baixo ou é muito magro, voce pode abaixar as gorduras para 0.35g de massa magra em libras ou aproximadamente 0,75g por massa magra em kilogramas Note 1: gorduras ''boas'' ou ''essencial'' nao equivalem ao total de gorduras ingeridos, porem sao incluidas no total, pois muitos alimentos possuem em si gorduras Note 2: Para aqueles em dietas de baixo carboidratos ou possuem necessidades especiais, a ingestao de gorduras é maior do que esse valor, podendo até ser maior que valories como 1g por massa magra em libras ou 2,2g por massa magra em kilogramas3. Carbs: Carboidratos sao os nutrientes menos essenciais, porem podem desempenhar um grande papel em uma dieta, eles ajudam a dar energia, manter a sanidade e saciedade, e também pode ajudar alguns individuos em termos de obtencao de energia Para o calculo de carboidratos é muito fácil, pois serao usadas as calorias que sobraram apos calcular os dois principais nutrientes, que sao gorduras e proteinas Para o calculo voce usara a seguinte formula: Caloria dos carboidratos = Calorias total - [proteina em gramas x 4] - [gorduras em gramas x 9] Apó obter a caloria dos carboidratos, voce dividirá por 4, pois cada grama de carboidrato possui 4kcal(fibras podem variar no valor, mas é recomendável que sempre calcule fibras como 4kcal, pois o valor é realmente variavel e nao há como saber realmente, e também para manter algo instável e seguro. Ou seja, Caloria dos carboidratos / 4 = Carboidratos em gramas Fonte: http://www.emma-leig...orie_needs.htmlExemplo: -Um homem de 100kg com 20% de BF -Calorias para manter(TMB): 3000kcal -Calorias para o cut: 2400kcal -1.5g proteina por lb/MASSA MAGRA....seria mais ou menos 3 à 3,3 g/kg: (1.5 * 160) 240g -0.45g gordura por lb/MASSA MAGRA: (200 * 0.45) 90g -Calorias da proteinas + gordura Minimas: (240 * 4) + (90 * 9) = 1770kcal -Calorias mínimas de sobra: (2400 - 1770)= 630kcal -Ele ainda possui 630kcal para colocar em comidas que QUISER e ainda continuara a perder gordura Ok, parece facil, mas existem dicas e fundamentos para seguir essa dieta sem fazer uma dieta porca.Dicas: -Consuma MUITOS nutrientes de comidas NAO PROCESSADAS, pois elas possuem os micronutrientes necessarios para manter uma SAUDE boa.... -Divide suas refeicoes de acordo com a sua preferencia, 3 ou 6 refeicoes por dia da na mesma, se vc atingir os macros.... -Temporizar seus nutrientes nao é necessarios.Nao existe nenhuma necessidade de colocar algo especifico no pre e pos, como evitar gordura ou etc. De toda maneira, micronutrientes, macronutrientes e o consumo calorico é de longe o mais importante. Um video em ingles: Epero que voces leiam e pensem antes de sair trollando, nao quis de maneira alguma falar mal, apenas alertar voces de que muita coisa que vcs acreditam, seguem, esta errada. Muita gente comendo albumina, muitos shakes, so para tentar alcancar um objetivo. Deixa de consumir chocolate, cereal, sorvete para ficar no franguinho com batata....por favor, abram suas mentes e pensem mais antes de ficar colocando dietas e mais dietas para avaliacao, pensem nos seus macros, calorias e etc, ao inves de postar todo plano calorico, por que nao postar apenas a separacao dos macronutrientes, e la vc coloca o que quiser, com SUA sabedoria... IIFYM é a melhor coisa se souber ser seguida, ou seja, usar sua conciencia e fazer uma dieta equilibrada entre alimentos nao limpos ou limpos, se é que isso existe, porque no final viram a mesma coisa....Mas como vou controlar minha dieta? Aconselho a voce usar um dos calculadores online, ou até mesmo uma tabela excel para isso, como a que existe aqui no site, os mais famosos e corretos sao:http://caloriecount.about.com/http://www.myfitnesspal.com/http://fatsecret.com/ Para quem preferir uma tabela excel, esse site é ótimo;http://nutritiondata.self.com/ É sempre bom buscar mais de uma fonte de pesquisa, para ter certeza, sempre conferir MACRONUTRIENTES, nao apenas calorias, pois muitos valores de embalagens podem estar errados, como o controle sobre calorias de fibras, que podem variarSite com receitas muito criativas e ''saudáveis'' : Food GawkerSheila's LiveWell 360Food of AprilFor The Love Of Cookies!Teresa Cutter - The Healthy Chef!Susan Jane Murray - Eating with IntolerencesPimp My ProteinShake!Diet, Desserts, and Dogs!Heather Eats Almond ButterKath Eats Real FoodPeanut Butter BoyStuff I make my HusbandPimp My Protein ShakeCouched Estudos científicos comprovando alguns fatos:Frequencia alimentar nao afeta o metabolismo, ou seja, nao precisa comer de 3 em 3 horas: http://www.ncbi.nlm....pubmed/19943985 This study shows there was no difference in weight loss between subjects with high/low meal frequencies.http://www.ncbi.nlm..../pubmed/9155494 Evidence supports that meal frequency has nothing to do with energy in the subjects.http://www.ncbi.nlm....pubmed/11319656 Yet again, no difference in energy in the subjects compared to 2 meals/d to 6 meals/d.And if you want to do some more detailed digging, you can read:http://www.ncbi.nlm..../pubmed/1905998 Eur J Clin Nutr. 1991 Mar;45(3):161-9.Links Influence of the feeding frequency on nutrient utilization in man: consequences for energy metabolism.http://www.ncbi.nlm....pubmed/11319656 Int J Obes Relat Metab Disord. 2001 Apr;25(4):519-28.Links Compared with nibbling, neither gorging nor a morning fast affect short-term energy balance in obese patients in a chamber calorimeter.http://www.ncbi.nlm....pubmed/18053311 Br J Nutr. 2008 Jun;99(6):1316-21. Epub 2007 Dec 6. Links Acute effects on metabolism and appetite profile of one meal difference in the lower range of meal frequency.http://www.ncbi.nlm..../pubmed/1905998 Eur J Clin Nutr. 1991 Mar;45(3):161-9.Links Influence of the feeding frequency on nutrient utilization in man: consequences for energy metabolism.http://www.ncbi.nlm....pubmed/11319656 Int J Obes Relat Metab Disord. 2001 Apr;25(4):519-28.Links Compared with nibbling, neither gorging nor a morning fast affect short-term energy balance in obese patients in a chamber calorimeter.http://www.ncbi.nlm....pubmed/18053311 Br J Nutr. 2008 Jun;99(6):1316-21. Epub 2007 Dec 6. Links Acute effects on metabolism and appetite profile of one meal difference in the lower range of meal frequency.http://www.ncbi.nlm..../pubmed/9155494 Br J Nutr. 1997 Apr;77 Suppl 1:S57-70. Links Meal frequency and energy balance.http://www.ncbi.nlm....pubmed/15806828 Forum Nutr. 2003;56:126-8.Links Highlighting the positive impact of increasing feeding frequency on metabolism and weight management.http://www.ncbi.nlm..../pubmed/9504318 Int J Obes Relat Metab Disord. 1998 Feb;22(2):105-12.Links Evidence that eating frequency is inversely related to body weight status in male, but not female, non-obese adults reporting valid dietary intakes.http://www.ncbi.nlm....pubmed/15085170 Int J Obes Relat Metab Disord. 2004 May;28(5):653-60. Links Decreased thermic effect of food after an irregular compared with a regular meal pattern in healthy lean women.http://www.ncbi.nlm....pubmed/15220950 Eur J Clin Nutr. 2004 Jul;58(7):1071-7. Links Regular meal frequency creates more appropriate insulin sensitivity and lipid profiles compared with irregular meal frequency in healthy lean women.http://www.ncbi.nlm....pubmed/17228037 Obesity (Silver Spring). 2007 Jan;15(1):100-6. Links Association of eating frequency with body fatness in pre- and postmenopausal women.http://www.ncbi.nlm....pubmed/15640455 Am J Clin Nutr. 2005 Jan;81(1):16-24. Links Comment in: Am J Clin Nutr. 2005 Jan;81(1):3-4. Beneficial metabolic effects of regular meal frequency on dietary thermogenesis, insulin sensitivity, and fasting lipid profiles in healthy obese women.http://www.ncbi.nlm....pubmed/10578205 Int J Obes Relat Metab Disord. 1999 Nov;23(11):1151-9.Links Acute appetite reduction associated with an increased frequency of eating in obese males. Mas eu achei estudos do International Society of Sports Nutrition (ISSN) sobre frequencia alimentar, e eles sao confiáveis, nao? Sugiro que leia o Review do Alan Aragon: A Critique of the ISSN Position Stand on Meal Frequency By Alan Aragon www.alanaragon.com www.alanaragonblog.com/aarr Originally Presented at Leangains.com, April 4th, 2011IntroductionThe International Society of Sports Nutrition (ISSN) is a forerunner in the movement toward providing reliable nutrition information for sports and fitness professionals. By virtue of its academically decorated staff and peer-reviewed research journal (JISSN), the ISSN is in a justifiable position to consider itself one of the world’s top authorities on sports nutrition. Thus, when they issue a position statement on any given topic, it’s frequently cited as solid evidence, and not taken lightly. For example, along with other literature reviews, I regularly cite their position paper on protein requirements for athletes . However, I typically follow that up with what I do in personal practice, which isn’t always research-backed. It’s important to keep an eye on both the research and the trenches, since field knowledge can take years and sometimes decades to make it into academic publication.It’s clear that the focus of their latest position stand is meal frequency’s effect on body composition. Right from the start, the authors illustrate the importance of this topic by citing the obesity epidemic in the United States. Setting the tone as such implies that weight/fat loss is the most pressing concern of the position stand, more so than other aspects such as muscle gain and exercise performance. This focus is justified, given the prevalence of obesity in industrialized nations, not just the United States. This justification is bolstered by the myriad health complications that accompany a chronic state of excess body fat. The next question becomes, how well does the ISSN support their meal frequency assertions to this end? I encourage you to have the ISSN’s position stand open while you read through this critique of the evidence used to support their key claims. The full text of the paper is freely available, see the reference list . Body Weight & Body CompositionThe authors begin the above-titled section by discussing uncontrolled/observational studies, including animal data. We can safely skip those, since the threats to their validity are numerous & obvious. They then move on to discuss experimental studies in humans. They correctly note that on the whole, the evidence in this area fails to indicate the superiority of increased meal frequency for improving weight loss. An interesting and important detail is the authors’ point that the minority of studies that did show improvements as a result of increased meal frequency happened to be in athletic subjects, whereas the ones that did not examined overweight/obese subjects. Three studies were provided to support this, which I’ll discuss next.First up is Benardot et al, who compared the effects of three 250 kcal between-meal snacks with a noncaloric placebo . A significant increase in anaerobic power and lean mass was seen in the snacking group, with no such improvements seen in the placebo group. Obviously, it’s impossible to credit the superior results to a higher meal frequency since this was also accompanied by a higher overall energy intake. The next study cited was by Deutz et al, which was not a controlled comparison of the isolated effects of different meal frequencies . Instead, it merely drew correlations between body composition and the results of a 24-hour recall of diet and physical activity variables. The final study was by Iwao et al, who found that boxers consuming 6 meals a day lost less lean body mass (LBM) and showed lower molecular measures of muscle catabolism than the same diet consumed in 2 meals per day .Of the three aforementioned studies, one was correlational. Of these two studies that demonstrated causation, only one of them (the boxer study) equally matched the intakes of each group. However, its design flaws compromise its relevance. Aside from flaws common to studies on both sides of the fence (short trial duration, subpar assessment methods, small sample size), the total energy intake at 1200 kcal was artificially low compared to what this population would typically carry out in the long-term. It’s also important to note that the protein intake, at 20% of total kcals, amounted to a paltry 60g/day. This translated to slightly under 1.0g/kg. To illustrate the inadequacy of this dose, recent research by Mettler et al showing that protein as high as 2.3g/kg and energy intake averaging 2022 kcal was still not enough to completely prevent LBM loss in athletes under hypocaloric conditions . Therefore, the ISSN’s claim that increased meal frequency in athletic populations may improve body composition is based on a single study with questionable applicability.Missing Research on Body Composition In addition to the aforementioned limitation, the authors failed to mention research that runs contrary to their assertion that, “Interestingly, when improvements in body composition are reported as a result of increasing meal frequency, the population studied was an athletic cohort.” Introducing the topic of comparative drops in LBM opens up a can of worms that does not support the ISSN’s claims. A recent review by Farady concluded that although daily caloric restriction (DCR) and intermittent calorie restriction (ICR) have similar effects on total bodyweight reduction, ICR has thus far been more effective for retaining lean mass . The results of 11 DCR studies 7 ICR studies were clearly laid out. Here are a couple of key stats that contributed to Farady’s conclusion:3 of the ICR studies showed no significant decrease in LBM, while all of the DCR studies showed decreases in LBM. In studies lasting 8-12 weeks, average LBM loss was 1.25% in ICR and 4% in DCR.Adding to the body of contrary data to the ISSN’s position, there are two more studies showing the superior effects on LBM status via lower meal frequency. An 8-week trial by Stote et al found the group consuming one meal per day gained lean mass and lost body fat, while the group consuming 3 meals per day showed no improvements in body composition . It should be noted that just like the study by Iwao et al, Stote et al’s results are limited by the use of BIA to assess body composition. Oyvind et al compared the 12-week effects of eating 3 versus 6 meals per day in subjects on a resistance training program, and the lower-frequency group gained significantly more LBM .Collectively, this body of research refutes the ISSN’s claim that superior effects on body composition have only been seen in athletic subjects with higher meal frequencies.Blood Markers of HealthAs an obligatory introduction, the authors begin their above-titled section by discussing observational/uncontrolled studies. Again, there’s no need to wade through this, given the availability of controlled studies. The first controlled intervention discussed is by Stote et al, where blood pressure and total cholesterol (both HDL & LDL) were higher in the group consuming 1 meal per day compared to the 3-a-day group . However, Stote et al noted that the difference in blood pressure may have been due to differences in circadian rhythm since it was measured in the late afternoon in the 1-meal group, and in the early morning in the 3-meal group. No speculations were made over what might have caused the cholesterol increase in the 1-meal group.Another concern of the ISSN was the potentially adverse effect of lower meal frequency on glucose homeostasis. In support, they cited work published in the 1960’s. They also cited subsequent work done in the same proximity with contrary outcomes. Notably, they discussed a study by Jenkins et al, which compared 3 versus 17 feedings per day and found no difference in mean blood glucose levels . Although the latter failed to show improvements in blood glucose levels, benefits from the (unrealistically) high meal frequency improved insulin levels and blood lipid profile. Although the data in this area is equivocal, the ISSN recommends increasing meal frequency for the purpose of improving health markers.Missing Research on Glucose ControlAn 8-week trial by Carlson et al found that subjects consuming 3 meals instead of 1 meal per day had more favorable results on an oral glucose tolerance test (OGTT) . However, the authors of this study acknowledge that this may have been due to a much larger consumption of food in closer proximity to the OGTT in the single-meal group. Testing was first thing in the morning, and the single-meal group consumed their day’s intake in a 4-hour window before bed.A very recent study adds to the evidence contrary to this idea, and was likely unavailable at the time of the ISSN position stand was written. Holmstrup et al found that glucose levels remained elevated throughout the day with frequent 6 meals compared to 3 meals, and no differences in insulin levels were seen . The key design strengths this study has over predecessors were the frequent sampling used to track blood glucose and insulin levels, and the use of healthy non-obese subjects with normal glucose tolerance. These aspects make it more relevant to active & athletic populations, to whom the ISSN’s position stand is directed in the first place. Another trial too recently published to make it into the position stand was by Harvie et al, who found that intermittent energy restriction was as effective as continuous energy restriction for decreasing bodyweight and increasing insulin sensitivity .In sum, due to the inconsistency of the data, it appears that increasing meal frequency for the purpose of improving health-related biomarkers is a premature recommendation. MetabolismThe aspects of metabolism discussed in this section are diet-induced thermogenesis (DIT – also called the thermic effect of food), resting metabolic rate, and protein metabolism. As for DIT, differences between varying meal distributions across several studies are negligible. The same lack of difference was also seen in several studies, including tightly controlled designs involving metabolic chambers to measure resting metabolic rate and total energy expenditure. These data further serve to invalidate the dying cliché of stoking the metabolic fire with frequent small feedings.The discussion of protein metabolism mainly involved the effects of meal frequency on nitrogen retention. The ISSN duly notes that most studies discussed in this section used nitrogen status as a proxy for muscle protein status, which is not always reliable. The nitrogen balance technique measures whole-body (systemic) nitrogen flux, rather than directly measuring protein turnover within skeletal muscle. Although the nitrogen balance method has limited applicability, it provides clues & hypotheses to test through more rigorous & direct means. The literature on meal frequency and nitrogen retention is reviewed, and the bulk of the data shows no differences despite meal frequencies ranging from one to six meals per day.The discussion of effects on protein metabolism begins by citing work by Garrow et al, who saw less nitrogen loss in obese subjects in hypocaloric conditions consuming 5 meals per day, compared to consuming 1 meal per day, and lean mass preservation was more pronounced in the higher protein treatments . However, the extrapolability of this research to real-world scenarios in non-sedentary & athletic populations is highly questionable. Total energy of the diets was 800 kcal, and the protein levels tested ranged from 10-15% of total kcals, amounting to 20-30g of protein per day. This amount represents about a tenth of the protein typically consumed by adult male athletes. The limitations of this study’s design are obvious.The authors then proceed down a slippery slope by discussing the potential benefit of maximizing muscle protein synthesis (MPS) on a per-meal basis. In acute (short-term or immediate-effect) studies on individuals of average body weight, the protein dose that tops out MPS is roughly 20-30g of high-quality protein, or about 10-15g of essential amino acids (EAA). Given this, the authors make a logical leap by presuming that more frequent occasions of maxing-out MPS would ultimately lead to faster rates of muscle gain. To support this idea, they cite rodent research by Wilson et al  and short-term human research by Paddon-Jones et al . I’ll comment on the latter since rat data pales in relevance when there’s human data available to examine. Paddon Jones et al found that MPS was greater when an EAA + carbohydrate liquid supplement was consumed between the 3 regular-sized solid meals . As a result, this study is often cited to support both the idea of increasing protein feedings as well as the benefits of dosing EAA between meals. The problem is, the group receiving the inter-meal supplementation ended up with 45g EAA + 90g carbs more than the control group by the end of the 16-hour test period. This treatment imbalance in both total calories and macronutrition is compounded by low protein intakes, averaging 23g per meal, totaling 64g per day. The experimental group’s supplemental intake boosted protein intake to 109g. So, not only was there the confounding element of unmatched macronutrition between groups, it essentially was a comparison of insufficient protein intake versus barely adequate intake.After examining the literature on protein metabolism/nitrogen retention, the ISSN concluded that, “…it appears as if the protein content provided in each meal may be more important than the frequency of the meals ingested, particularly during hypoenergetic intakes.” Still, this statement is collectively based on the Garrow study involving 20-30g protein per day, the Wilson rodent study, and the Paddon-Jones study, all of whose limitations are critical. Nevertheless, the ISSN made the redeeming point that increasing meal frequency isn’t likely to increase metabolic rate. To their credit, they repeatedly acknowledged that there’s a lack of research on the effect of meal frequency on various aspects of metabolism in athletic & physically active subjects. Missing Research on Markers of Protein MetabolismMissing from this section of the paper was any mention of recent work by Soeters et al, who saw no difference in glucose, lipid, or protein metabolism between an intermittent fasting treatment (involving 20-hour fasting cycles) and a standard diet . Similarly, Arnal et al saw no significant difference in body composition & nitrogen retention in subjects consuming most of their daily calories in 1 meal versus 4 evenly-spread meals throughout the day . In older subjects, the same research team actually found better nitrogen retention with most of the day’s calories from 1 meal instead of 4 meals .Although the ISSN isn’t firm with it, there’s an underlying implication that increasing the frequency of protein dosing at the threshold known to max-out MPS (20-30g protein or 10-15g EAA) would optimize the rate of net muscle protein gains. If this were true, then more muscle would be lost in lower-frequency treatments. Conversely, greater gains would be seen in higher-frequency treatments over time. The majority of the research thus far has simply not supported either one of these phenomena [7-9, 17-19, 21, 22]. Hunger and SatietyThis section begins by discussing short-term (within-day) effects of meal frequency on hunger and satiety. These designs involved the pre-loads of varying meal distributions, and measuring subsequent ad libitum food intake. Unanimously, the higher-frequency meal preloads resulted in better appetite control, evidenced by lesser subsequent intakes. Additionally, a study by Smeets et al found higher satiety ratings over a 24-hour period in subjects consuming 3 meals instead of 2 .The important question is whether the hunger-controlling effects of higher meal frequency persist beyond a single day. The ISSN only mentions 2 such studies, and they happen to have conflicting outcomes. Stote et al’s 8-week trial reported greater hunger levels in subjects consuming 1 versus 3 meals per day . A more recent trial by Cameron et al compared 6 meals per day (technically 3 meals + 3 snacks) with 3 meals per day, and found no significant differences in appetite ratings . Additionally, there were no trends suggesting a significant effect of increased meal frequency on the levels of the appetite-regulating peptides ghrelin and peptide YY (PYY). As seen consistently in other research, there were no differences bodyweight decrease or body composition change. Curiously, despite the equivocal results of these two trials, the ISSN concluded that increasing meal frequency is likely to decrease hunger and control intake in subsequent meals. But as we’ll see, more recent data continues to challenge this idea. Missing Longer-Term Research on Hunger & SatietyAn important study is missing from the ISSN’s review. In fairness, it’s likely because it wasn’t yet available at the time it was written. Leidy et al compared varying protein levels consumed across either 3 or 6 meals per day . Predictably, the higher-protein level (25% vs. 14%) promoted greater satiety. Interestingly, the higher meal frequency led to lower daily fullness ratings regardless of protein level. Meal frequency had no significant impact on ghrelin levels, regardless of protein intake. PYY, which is associated with satiety, was 9% lower in the higher meal frequency.When focusing mainly on the short-term (within-day) studies, increasing meal frequency appears to have beneficial effects on appetite control. However, these results for the most part have not been supported by longer-term research. Thus, the blanket recommendation to increase meal frequency in order to decrease hunger is not based on the weight of the evidence.Athletic PopulationsThis section of the position paper was basically a reiteration of the outcomes of 3 studies discussed earlier, in attempt to emphasize the point that more is potentially better when it comes to meal frequency. In response, I’ll briefly review my contentions with the applicability of this data. Deutz et al was a retrospective correlational study, not a controlled intervention capable of demonstrating causation . Iwao et al’s study on boxers used a protocol that was artificially low in total kcals and unrealistically low in protein compared to what athletes typically consume . Benardot et al’s design did not match total energy and macronutrition between groups, so it’s not surprising that the greater performance and lean mass gains occurred in the group with the higher fuel consumption . In addition to the crucial limitations of these studies, research with contrary results (and equal or better design quality) is missing from this position stand [7-9].The authors go on to assert that data on the eating habits of competitive athletes (in primarily endurance-based sports) shows a range of roughly 5-10 eating occasions per day. They suggest that this is optimal because it enables athletes to consume a culturally normal meal pattern in addition to meals proximal to the training bout. In response to this, I’d say that this range of frequencies is fine for this population. But, I’d also contend that the energy needs of competitive athletes in endurance-based sports can be 2-4 times greater than that of recreationally active individuals (who make up the bulk of the nonsedentary adult population). Therefore, applying the meal frequency of competitive athletes to less active populations is unnecessary & impractical, at best. In my private practice, I’ve seen recreational athletes succeed long-term with as little as 2 meals per day. The most common meal frequency range I’ve observed in physically active clients with long-term success is rather broad (3-6 meals per day). Whether individuals choose the higher or lower end of that range is based solely on personal preference and tolerance. Boiling Things Down: The Position StatementsCredit is due to the ISSN for preemptively stressing that the research on physiological & morphological effects of meal frequency in physically active and athletic populations is scarce. They responsibly state that this prevents definitive conclusions from being made. The following are the exact statements that comprise the ISSN position stand on meal frequency, which I’ll follow with my comments & conclusion.Increasing meal frequency does not appear to favorably change body composition in sedentary populations. If protein levels are adequate, increasing meal frequency during periods of hypoenergetic dieting may preserve lean body mass in athletic populations. Increased meal frequency appears to have a positive effect on various blood markers of health, particularly LDL cholesterol, total cholesterol, and insulin. Increased meal frequency does not appear to significantly enhance diet induced thermogenesis, total energy expenditure or resting metabolic rate. Increasing meal frequency appears to help decrease hunger and improve appetite control.When examining the above points, 1 & 4 have a substantive, cohesive, and adequately-designed body of research backing them. Thus, they possess the strongest evidence basis of the bunch. Number 3 sits right on the fence, since it’s a particularly complex and delicate area with much conflicting data. It’s my hunch that the differential effects of varying meal frequencies on blood markers of health would greatly diminish in the presence of a formal exercise program. Again, the potentially profound impact of training that’s missing from the current meal frequency research leaves big questions unanswered. Points 2 & 5 have the least scientific support, and the largest leaps of faith and bias from the ISSN.In ClosingI’d advise everyone with enough motivation to dig into the references and question the conclusions of all parties involved. It’s clear that position stands of authoritative organizations are far from being completely accurate, complete, and bias-free. With that said, the ISSN provides plenty of food for thought. Again, read the full text of their paper in order to get the most out of my critique of it . Meal frequency research is becoming increasingly more active, so it’s safe to predict that in the coming years, more relevant designs will narrow the gap between the questions and answers. Something I can wholeheartedly agree with is the paper’s closing quote: “Nonetheless, more well-designed research studies involving various meal frequencies, particularly in physically active/athletic populations are warranted.”References1. Campbell B, et al. International Society of Sports Nutrition position stand: protein and exercise. J Int Soc Sports Nutr. 2007 Sep 26;4:8. [Medline] 2. La Bounty PM, et al. International Society of Sports Nutrition position stand: meal frequency. J Int Soc Sports Nutr. 2011 Mar 16;8(1):4. [Epub ahead of print] [Medline] [JISSN] 3. Benardot D, et al. Between-meal energy intake effects on body composition, performance, and total caloric consumption in athletes. Med Sci Sports Exerc. 2005;37(5):S339. [MSSE] 4. Deutz RC. et al. Relationship between energy deficits and body composition in elite female gymnasts and runners. Med Sci Sports Exerc. 2000 Mar;32(3):659-68. [Medline] 5. Iwao S, et al. Effects of meal frequency on body composition during weight control in boxers. Scand J Med Sci Sports. 1996 Oct;6(5):265-72. [Medline] 6. Mettler S, et al. Increased protein intake reduces lean body mass loss during weight loss in athletes. Med Sci Sports Exerc. 2010 Feb;42(2):326-37. [Medline] 7. Varady KA. Intermittent versus daily calorie restriction: which diet regimen is more effective for weight loss? Obes Rev. 2011 Mar 17. [Epub ahead of print] [Medline] 8. Stote KS, et al. A controlled trial of reduced meal frequency without caloric restriction in healthy, normal-weight, middle-aged adults. Am J Clin Nutr. 2007 Apr;85(4):981-8. [Medline] 9. Oyvind H, et al. The effect of meal frequency on body composition during 12 weeks of strength training. 12th Annual congress of the European College of Sport Science, 2007. [ECSS] 10. Jenkins DJ, et al. Nibbling versus gorging: metabolic advantages of increased meal frequency. N Engl J Med. 1989 Oct 5;321(14):929-34. [Medline] 11. Carlson O, et al. Impact of reduced meal frequency without caloric restriction on glucose regulation in healthy, normal-weight middle-aged men and women. Metabolism. 2007 Dec;56(12):1729-34. [Medline] 12. Holmstrup ME, et al. Effect of meal frequency on glucose and insulin excursions over the course of a day. Eur e-J Clin Nutr Metab. 2010 Dec;5(6):277-80. [e-SPEN] 13. Harvie MN, et al. The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women. Int J Obes (Lond). 2010 Oct 5. [Epub ahead of print] [Medline] 14. Garrow JS, et al. The effect of meal frequency and protein concentration on the composition of the weight lost by obese subjects. Br J Nutr. 1981 Jan;45(1):5-15. [Medline] 15. Wilson GJ, et al. Equal distributions of dietary protein throughout the day maximizes rat skeletal muscle mass. The FASEB Journal, 2010. 24(740.17). [FASEB J] 16. Paddon-Jones D, et al. Exogenous amino acids stimulate human muscle anabolism without interfering with the response to mixed meal ingestion. Am J Physiol Endocrinol Metab. 2005 Apr;288(4):E761-7 [Medline] 17. Soeters MR, et al. Intermittent fasting does not affect whole-body glucose, lipid, or protein metabolism. Am J Clin Nutr. 2009 Nov;90(5):1244-51. [Medline] 18. Arnal MA, et al. Protein feeding pattern does not affect protein retention in young women. J Nutr. 2000 Jul;130(7):1700-4. [Medline] 19. Arnal MA, et al. Protein pulse feeding improves protein retention in elderly women. Am J Clin Nutr. 1999 Jun;69(6):1202-8. [Medline] 20. Smeets AJ, Westerterp-Plantenga MS. Acute effects on metabolism and appetite profile of one meal difference in the lower range of meal frequency. Br J Nutr, 2008. 99(6): p. 1316-21. [Medline] 21. Cameron JD, et al. Increased meal frequency does not promote greater weight loss in subjects who were prescribed an 8-week equi-energetic energy-restricted diet. Br J Nutr. 2010 Apr;103(8):1098-101. [Medline] 22. Leidy HJ, et al. The influence of higher protein intake and greater eating frequency on appetite control in overweight and obese men. Obesity (Silver Spring). 2010 Mar 25. [Epub ahead of print] [Medline]Fonte: http://www.leangains...nd-on-meal.html Voce NAO precisa de um shake de ''rapida absorcao'', pois a janela anabólica dura 24 HORAS Por Alan Aragon: The postexercise "anabolic window" is a highly misused & abused concept (which I believe Layne agrees with). Preworkout nutrition all but cancels the urgency, unless you're an endurance athlete with multiple glycogen-depleting events in a single day. Getting down to brass tacks, a relatively recent study (Power et al. 2009) showed that a 45g dose of whey protein isolate takes appx 50 minutes to cause blood AA levels to peak. Resulting insulin levels, which peaked at 40 minutes after ingestion, remained at elevations known to max out the inhibition of muscle protein breakdown (15-30 mU/L) for 120 minutes after ingestion. This dose takes 3 hours for insulin & AA levels to return to baseline from the point of ingestion. The inclusion of carbs to this dose would cause AA & insulin levels to peak higher & stay elevated above baseline even longer. So much for the anabolic peephole & the urgency to down AAs during your weight training workout; they are already seeping into circulation (& will continue to do so after your training bout is done). Even in the event that a preworkout meal is skipped, the anabolic effect of the postworkout meal is increased as a supercompensatory response (Deldicque et al, 2010). Moving on, another recent study (Staples et al, 2010) found that a substantial dose of carbohydrate (50g maltodextrin) added to 25g whey protein was unable to further increase postexercise net muscle protein balance compared to the protein dose without carbs. Again, this is not to say that adding carbs at this point is counterproductive, but it certainly doesn't support the idea that you must get your lightning-fast postexercise carb orgy for optimal results. Estudos científicos: nother common thing I hear... You MUST IMMEDIATELY take a fast-digesting protein, such as whey, prior to working out to stimulate the best gains.http://www.ncbi.nlm....pubmed/21045172 This study showed that immediate responses to whey and casein ingestion were different... But the end result was the same. They both stimulated protein synthesis equally.http://www.ncbi.nlm....pubmed/15570142 This study shows almost exactly the same thing. Both proteins caused equal protein synthesis. These findings are only compounded by having solid pre workout nutrition. A quote by Alan Aragon states: "Properly done preworkout nutrition EASILY elevates insulin above and beyond the maximal threshold seen to inhibit muscle protein breakdown. This insulin elevation resulting from the preworkout meal can persist long after your resistance training bout is done. Therefore, thinking you need to spike anything is only the result of neglecting your preW nutrition" Myth, again, DENIED! You do not need a fast-digesting protein immediately postworkout. Nor do you need ANY protein post workout provided you are not lifting in a fasted state. O corpo nao tem limite de absorcao de proteínas por refeicao http://www.hipertrof...unica-refeicao/http://www.wannabebi...-a-single-meal/ Indice Glicemico nao importa ao menos que voce tenha Diabetes http://www.ncbi.nlm....Pubmed_RVDocSumhttp://weightology.n...ly/?page_id=319http://www.ncbi.nlm....Pubmed_RVDocSumhttp://fitnfly.com/l...trition-facts-2 Pre, Pós e Durante treino, o que comer? Hierarchy of Importance When speaking of nutrition for improving body composition or training performance, it's crucial to realize there's an underlying hierarchy of importance. At the top of the hierarchy is total amount of the macronutrients by the end of the day. Distantly below that is the precise timing of those nutrients. With very few exceptions, athletes and active individuals eat multiple times per day. Thus, the majority of their day is spent in the postprandial (fed) rather than a post-absorptive (fasted) state. The vast majority of nutrient timing studies have been done on overnight-fasted subjects put through glycogen depletion protocols, which obviously limits the applicability of the outcomes. Pre-exercise (and/or during-exercise) nutrient intake often has a lingering carry-over effect into the post-exercise period. Throughout the day, there's a constant overlap of meal digestion & nutrient absorption. For this reason, the effectiveness of nutrient timing does not require a high degree of precision.The Primary Laws of Nutrient Timing The First Law of Nutrient Timing is: hitting your daily macronutrient targets is FAR more important than nutrient timing. The Second Law of Nutrient Timing is: hitting your daily macronutrient targets is FAR more important than nutrient timing.http://user210805.we...RR-Jan-2008.pdf Carboidratos depois das 6 horas da tarde NAO te engordam:http://www.leangains...er-for-fat.htmlPular o café da manha NAO te engorda:http://www.leangains...s-debunked.htmlGordura Saturada NAO é uma vila como diziam: -Results from prospective studies show few effects. Very low consumption of saturated fat possible increases risk of intraparenchymal hemorrage, and high consumption of processed/vegetable trans fat possibly increases CHD risk. Both findings should be interpreted with care since no evidence was found for an association with total CVD. Suggestive evidence was found that dietary cholesterol intake increases CVD risk. This association should also be interpreted with care since no evidence was found for an association with either CHD or stroke. Inconclusive evidence was found for an association between any other type of dietary fat and any type of CVD. -Results from prospective studies show that full-fat dairy items and low-fat dairy items do not consistently differ in their effects on CVD. Certainly, no conclusion can be drawn that margarine intake decreases CHD rates relative to butter. No data is available about the relation between meat fats and CVD. -Analysis of randomized trials about substitution of dietary fats showed that a large amount of confounders was able to influence the effects on CVD. None of the intervention trials was able to isolate the effect from saturated fats on CHD. -Analysis of randomized trials about substitution of dietary fats showed that changes in serum cholesterol, caused by changes in dietary fat intake, are not predictive of CHD risk.-Analysis of the validity of conclusions from 3 advisory committees (Institute of Medicine. 2005; USDA/USDHHS. 2010; and EFSA. 2010) shows that all advisory committees ignored results from the majority of both randomized trials and prospective cohort studies. Effects from 'good' HDL-cholesterol on CVD, caused by saturated fat intake are ignored consistently. And true results from the scientific literature were manipulated to better fit advices in 2 out of 3 reports. Source: Dietary fat, dietary cholesterol, and cardiovascular disease. Canceranddiet.nl. Available at: http://canceranddiet...ietary-fat.htmlINTRODUCTION. Consumption of saturated fat increases levels of LDL- (bad) cholesterol. And LDL-cholesterol increases risk of heart disease. These correlations have led to worldwide recommendations to decrease consumption of saturated fat in order to decrease risk or heart disease. Generally, advisory committees/scientists use 3 types of support for these recommendations: 1) Results from randomized studies have shown that saturated fat consumption increases cholesterol levels. 2) Intervention studies have shown that the decrease of saturated fat, and simultaneous increase of polyunsaturated fat in the diet, decreases CHD risk. 3) Prospective cohort studies have shown that saturated fat intake increases coronary heart disease risk. All types of support will be discussed, and brought into perspective with data from other types of evidence.THEORY 1: RESULTS FROM RANDOMIZED STUDIES HAVE SHOWN THAT SATURATED FAT CONSUMPTION INCREASES CHOLESTEROL LEVELS. Often, advisory committees and scientists use the same article to prove that saturated fat intake negatively influences cholesterol: A meta-analysis of 60 randomized studies examined the effects of replacing carbohydrates by different types of fat (Mensink RP. 2003). The feeding studies included lasted between 13 and 91 days. What did this meta-analysis find? The analysis showed that replacing carbohydrates by saturated fat increased cholesterol levels, but contrary to what is often suggested, this effect is not necessarily disastrous. Both the levels of 'bad' LDL-cholesterol, and 'good' HDL-cholesterol increased significantly. Saturated fat consumption increased HDL-cholesterol to an even larger extend than both monounsaturated-, and polyunsaturated fat. Saturated fat significantly increased total cholesterol levels, but the ratio of total:HDL-cholesterol was not influenced. The authors found that replacing carbohydrates with any food source rich in dietary fats will improve the ratio total:HDL cholesterol:And the predicted changes were calculated:Do subjects with higher cholesterol levels have an increased risk of cardiovascular disease? A meta-analysis of 61 prospective studies examined the relation between cholesterol, and mortality from cardiovascular disease (Prospective Studies Collaboration. 2007). Subjects with higher cholesterol levels had a significantly increased risk of CHD mortality, but the ratio total:HDL-cholesterol was the strongest predictor of CHD mortality. And both HDL-cholesterol, and LDL-cholesterol levels were independent predictors of mortality from CHD. Is focusing on effects on cholesterol causes by increased saturated fat intake a reliable way to predict effects on heart disease? The researchers from the meta-analysis about effects of fat on the cholesterol (Mensink RP. 2003) warn against focusing on the effects of intermediate end point:They also warn against focusing on just one single intermediate end point:And long-term effects are unknown:Conclusion: Saturated fat consumption increases both HDL-, and LDL-cholesterol levels compared to carbohydrates, without changing the ratio total:HDL-cholesterol. Subjects with higher cholesterol levels probably have increased risk of mortality from CHD compared to subjects with lower cholesterol levels, but the ratio total:HDL-cholesterol was a much stronger predictor of this association. Dietary fats will probably - apart from their effects on cholesterol levels - also influence other intermediate end points for CHD, and how the sum of the different effects from the various intermediate end points will eventually influence risk of CHD, can not be predicted.THEORY 2: INTERVENTION STUDIES HAVE SHOWN THAT THE DECREASE OF SATURATED FAT, AND SIMULTANEOUS INCREASE OF POLYUNSATURATED FAT IN THE DIET, DECREASES CHD RISK. In the past years, several systematic reviews of randomized studies were published which looked at the effect of replacing saturated fat by polyunsaturated fat (Hooper L. 2000/2001; Skeaff CM. 2009; Mozaffarian D. 2010; Ramsden CE. 2010). Results of these systematic reviews can be seen in the following table. Studies examining the effects of polyunsaturated fat consumption from fish were mostly not included in these systematic reviews. Since results from all randomized trials were published well before the year 2000, all authors were able to include data from all available trials.Results from the 4 systematic reviews were similar for CVD/CHD risk, but differed for CVD/CHD mortality, and mortality from all causes. The 4 reviews included different randomized trials: -The Finnish Mental Hospital Trial (Turpeinen O. 1979; Miettinen M. 1983) was only included by Skeaff CM, and Mozaffarian D. In this trial, subjects were not randomized to the dietary trial group, or the control group on an individual level. Instead, all subjects in one hospital were allocated to the experimental group, while all subjects in another hospital were allocated to the control group. Six years later, the hospitals switched their diets. -The Rose Corn Oil Trial (Rose GA. 1965) was included in all reviews, except the one from Mozaffarian D. Except for this trial, Skeaff CM and Mozaffarian D included the same 7 trials. -The DART Study (Burr ML. 1989) was included in all reviews, except the one from Ramsden CE. This author stratified effects by differences in the type of dietary polyunsaturated fats included in the experimental diets. And the DART Study did not provide data about the specific n-6 and n-3 PUFA composition of the study diets. -The Sydney Diet-Heart Study (Woodhill JM. 1978) was only included by Hooper L, and Ramsden CE. The trial provided data about all-cause mortality, but not about CVD/CHD. But Ramsden CE pointed out that all-cause mortality increased by 49% in this study, and 61 of 67 deaths were attributed to CHD. Therefore, failure to publish the full dataset of this negative study probably led to an overestimation of the beneficial effects of cholesterol-lowering polyunsaturated fat diets on CHD. -Note: Results for mortality from all causes differed between Skeaff CM, and Mozaffarian D, while the same cohorts were included for this analysis. This may be caused by the possibility that Skeaff CM interpreted results from "The Finnish Mental Hospital Trial" incorrectly (Miettinen M. 1972). Skeaff CM found a significant protective effect against mortality (- 26% for men, and - 27% for women), while the authors from this trial themselves found no effect among women, and a small non-significant protective effect among men. It is possible that Skeaff CM overlooked the fact that the control group was followed for a longer period of time (3.13 y for women, and 2.93 y for men, respectively) compared to the invervention group (2.60 y for women, and 2.38 y for men, respectively. -Note: The analysis by Hooper L differed to a large extend from the analysis by Mozaffarian D, and Skeaff CM. More studies were included, while less subjects died. This is partly because no subjects got sick or died in 13 out of 27 included studies during the trial period, and this is partly because "The Finnish Mental Hospital Trial" was excluded from the analysis. The latter trial included 1,285 deaths from all causes.It seems that results from the "The Finnish Mental Hospital Trial" can explain the differences between the 4 systematic reviews to a large extend. This trial was excluded in 2 reviews (Hooper L. 2000; Ramsden CE 2010), end the size of the protective effect against all-cause mortality is probably overestimated in another review (Skeaff CM. 2009).Results from the 4 systematic reviews of randomized trials: All 4 reviews found a protective effect against risk of CVD/CHD from replacing saturated fat by polyunsaturated fat. Risk decreased by 15-19%. Hooper L (2000) showed that all effects lost significance when "The Oslo Diet-Heart Study" (Leren P. 1970) was excluded in which the intervention group was additionally randomized to fish consumption. This study was included in all 4 systematic reviews. After exclusion of this study the RR's became (0.86; 95% CI = 0.72-1.03 for CVD risk, 0.94; 95% CI = 0.79-1.11 for CVD mortality, and 1.02; 95% CI = 0.91-1.14 for mortality from all causes). Only one out of four systematic reviews found a nonsignificant protective effect against all-cause mortality from replacing saturated fat by polyunsaturated fat (Skeaff CM. 2009). And as can be seen above, the author probably overestimated the size of this effect. All other authors found no effect on all-cause mortality (RR's of 0.98, 0.99, and 1.02 for Mozaffarian D, Ramsden CE, and Hooper L, respectively). Does it matter which type of polyunsaturated fats is used to replace saturated fat? Ramsden CE showed that effects differed by type of polyunsaturated fats used for the substitution of saturated fats. RR's for all end points were > 1 when trials examining n-6 specific polyunsaturated fats (linoleic acid) were used, and RR's for all end points were < 1 when trials examining both n6 and n3 polyunsaturated fats (alpha-linolenic acid) were used:In all trials saturated fat intake lowered, while polyunsaturated fat intake increases. So which type of fat was responsible for the effect on CHD found in the systematic reviews? None of the 4 systematic reviews analyzed the probability that any of the given effects was caused by any specific type of dietary fat. At least in the articles mentioned above...... The systematic review by Hooper L was published twice (2000, 2001). The version mentioned above was published in 2000, and was included in the Cochrane Database. In 2001 the review was published again. And in this second version the author tried to explore the relation between change in proportion of total fat, saturated fat, polyunsaturated fat, and monounsaturated fat on cardiovascular events. This analysis showed no evidence for an effect by total fat, saturated fat, and polyunsaturated fat, while monounsaturated fat significantly increased risk of cardiovascular events. The author warns that these results should be treated with caution, but clearly this analysis does not fuel the hypothesis that saturated fat consumption plays a major part in risk of cardiovascular events.Can changes in serum cholesterol - which are caused by changes in consumption of dietary fat - predict subsequent changes in CHD in a reliable way? Randomized studies consistently showed that dietary changes, aimed at substitution of polyunsaturated fat for saturated fat, decreased serum cholesterol levels. A global look at the subsequent effect on CHD suggests that these decreased levels of serum cholesterol, often correspond fairly well with the predicted decrease in CHD rates. But when more detailed findings are taken into account, little evidence remains that changes in serum cholesterol created by changes in dietary fat intake are predictive of CHD rates. Full details about this analysis can be found here: http://canceranddiet...rated-fat.html. Results from randomized trials of substitution of dietary fats are often used to "prove" a causal relation between consumption of saturated fat and CHD. But can results from these trials be attributed to the changes in saturated fat intake, or could other dietary and non-dietary changes have contributed to these results? Various confounders were able to influence the effect of replacing saturated fats by polyunsaturated fats. Sometimes, experimental groups were randomized to a complete mediterranean diet, including increased consumption of vegetables and fruits. The effect of reduced trans fat intake in the experimental groups, is likely to have attributed to the protective effects against coronary heart disease in all 8 trials. Saturated fat was replaced by polyunsaturated fat in all trials, and dietary cholesterol intake correlated strongly to saturated fat intake. Subsequently, none of the trials involved in the analysis was able to isolate the effect from saturated fats on CHD. Full details about this analysis can be found here: http://canceranddiet...rated-fat.html.Conclusions by the authors from the 3 systematic reviews of randomized trials to decrease saturated fat consumption, and simultaneously increase polyunsaturated fat consumption: 1) In 2000 Hooper L published his systematic review in the Cochrane Database. The following recommendation was made:But neither in the "results", nor in the "discussion" part of the article is any information given that an examination was done of the specific part of saturated fat in this effect. This suggest that his conclusion was based on an assumption, rather than on actual research. In 2001 Hooper L published the same systematic review again and - as shown above - not saturated fat, but monounsaturated fat was found responsible for the increased risk of CVD events. This made the author come to another conclusion:2) In 2009, Skeaff CM concluded the following:Also, this author concluded that substitution of saturated fat for carbohydrates, probably will not effect CHD events, and fatal CHD (see table 4 in the related article). 3) In 2010, Mozaffarian D, concluded the following:4) In 2010, Ramsden CE did not mention the specific effect of saturated fat.Conclusion: In the past, several dietary interventions trials were done to decrease consumption of saturated fat, and simultaneously increase consumption of polyunsaturated fat. Systematic reviews of these trials show that such an intervention may decrease risk of CVD/CHD by 15-19%, but will probably not increase survival. When only randomized trials were included, and when dietary interventions with fish consumption were excluded, no significant associations were found of replacing saturated fat by polyunsaturated fat (- 14% for CVD risk, - 4% for CVD mortality, and + 2% for all-cause mortality). An analysis of randomized intervention trials showed that total fat, saturated fat, and polyunsaturated fat did not influence risk of CVD events. Instead, monounsaturated fat consumption was found to significantly increase risk of CVD events. Furthermore, changes in serum cholesterol, caused by changes in dietary fat intake are not predictive of coronary heart disease risk. Finally, a large amount of confounders was able to influence the effects on CVD from substitution of dietary fats. None of the intervention trials involved was able to isolate the effect from saturated fats on CHD.THEORY 3: PROSPECTIVE COHORT STUDIES HAVE SHOWN THAT SATURATED FAT INTAKE INCREASES CORONARY HEART DISEASE RISK. According to the Institute of Medicine, the majority of epidemiological studies have reported an association between saturated fat intake and risk of CHD (Institute of Medicine. 2005). This conclusion is based on incorrect citing of true results from these studies: http://canceranddiet...eport-2005.html In the past 3 systematic reviews of prospective studies were published, examining the relation between consumption of saturated fat and CHD or stroke (Skeaff CM. 2009; Mente A. 2009; Siri-Tarino PW. 2010). These were all published recently. In a fourth systematic review the effects of replacing saturated fat by other macronutrients were examined (Jakobsen MU. 2009).High vs low consumption of saturated fat: Results from the first three systematic reviews are shown in the table below. None of these reviews found a significant association with CHD or stroke of high vs low consumption of saturated fat. Replacing saturated fat by unsaturated fat or carbohydrates: In 2009, Jakobsen MU published a systematic review about the effects on CHD of replacing saturated fat by 3 other macronutrients. Eleven cohorts were included in this analysis. Replacement by polyunsaturated fat decreased both risk-, and mortality from CHD. Replacement by monounsaturated fat or carbohydrates increased CHD risk - but not CHD mortality - among men.Conclusion: In the past, 3 systematic reviews examined the effect of high vs low consumption of saturated fat on CHD or stroke. None of these reviews found a significant association. A fourth review shows the effect of lowering saturated fat is probably related to the nutrient it is replaced by. In this case polyunsaturated fat may decrease CHD risk and mortality, while monounsaturated fat and carbohydrates may increase CHD risk among men.MEAT FATS AND DAIRY FATS IN RELATION TO CARDIOVASCULAR DISEASE AND ALL-CAUSE MORTALITY. Previously, I examined the relation between both meat- and dairy fats in relation to both CVD and all-cause mortality, based on results from prospective studies (see elsewhere on my site). The literature search covered the period until may 25, 2010. In short, results are as follows:-Meat fats and CVD None of the articles presented data about the relation between lean meats vs fatty meats for any type of meat. -Dairy fats and CVD No consistent differences in effect were found between full-fat and low-fat versions of total dairy products, milk, and cheese. Butter and margarine were not independently related to CHD, but within cohort comparisons showed RR's were lower for butter than for margarine in 5 out of 6 cohorts. In contrast, margarine possibly protects against stroke mortality among women, and butter possibly increases risk of intracerebral hemorrhage. Other fat dairy products were not linked to increased CVD rates: Cheese possibly decreases risk of ischemic stroke, and cream might protect against the sum or CHD and stroke. -Meat fats and all-cause mortality No associations were found. -Dairy fats and all-cause mortality no evidence was found for a modifying effect of dairy-, milk-, and cheese fat on the association between the related items and mortality. And no evidence was found for a difference in effect between butter and margarine.Conclusion: Results from prospective studies show that full-fat dairy items and low-fat dairy items do not consistently differ in their effects on CVD. Certainly, no conclusion can be drawn that margarine intake decreases CHD rates relative to butter. No data is available about the relation between meat fats and CVD.ARE THE CONCLUSIONS FROM ADVISORY COMMITTEES, ABOUT THE RELATION BETWEEN SATURATED FAT AND CARDIOVASCULAR DISEASE, VALID? Advices are based on conclusions and summaries of findings from literature searches. Ideally, these literature searches cover all relevant data available, according to a predefined set of criteria. This is called a systematic review. By standard, a systematic review never excludes results from individual studies found without a clear motivation. As mentioned before, advisory committees include 3 types of data to judge the evidence relating saturated fat intake to cardiovascular disease:-Randomized trials examining the effect of saturated fat intake on serum cholesterol. -Randomized trials examining the effect of substitution of polyunsaturated fat for saturated fat in relation to cardiovascular disease. -Prospective cohort studies examining the direct effect of saturated fat intake on cardiovascular disease.If advisory committees want to make valid conclusions based on all available evidence, they have to use data from systematic reviews covering these 3 topics, or they have to do a systematic literature search themselves. The table below is an overview of the criteria used to judge the evidence linking saturated fat intake to CVD/CHD in 3 different reports. The reports included are as follows. Full details about missing data and incorrect citations in these reports can be seen by clicking on the related item:-The dietary reference intakes for macronutrients 2005, by the Institute of Medicine. Read: http://canceranddiet...eport-2005.html -The dietary guidelines for Americans 2010, by the USDA, and the USDHHS. Read: http://canceranddiet...eport-2010.html -The scientific opinion on dietary reference values for fats 2010, by the EFSA. Read: http://canceranddiet...eport-2010.htmlDid the 3 European and US reports include all data available? -The EFSA report based it's evidence for the relation between saturated fat intake and serum cholesterol on a systematic review of randomized trials (Mensink RP. 2003). Both other reports only included only a small amount of the available evidence. -All 3 reports mentioned that saturated fat intake increases serum LDL-cholesterol and that serum LDL-cholesterol increases risk of CVD/CHD. -Only 2 out of 3 reports mentioned that saturated fat intake increases serum HDL-cholesterol. All reports failed at mentioning that serum HDL-cholesterol decreases CVD/CHD risk. None of the reports discussed the reason for this. One report cited the effect of saturated fat intake on serum HDL-cholesterol incorrectly. -The EFSA report was the only report to include data from randomized trials about the effect of substitution of dietary fats in relation to CVD. It failed at defining results from available systematic reviews (Hooper L. 2000, 2001), and it failed at describing the true dietary interventions used in these trials. -All 3 reports failed at systematically reviewing the available results from prospective cohort studies. The EFSA report included just one single cohort study. Both other reports did not only fail to include data from all available cohorts, but they also failed at correctly citing the true results from this limited amount of data.Conclusion: None of the 3 European and US reports evaluated all available evidence. Instead most of the available evidene from both randomized trials and prospective cohort studies were ignored. Though 2 reports mentioned the fact that research has shown that saturated fat increases HDL-cholesterol to an even larger extend than unsaturated fats, none of the reports found it necessary to discuss the finding that HDL-cholesterol decreases CHD mortality (Prospective Studies Collaboration. 2007). Both US reports did not find it necessary to define results from prospective cohort studies, the way they were defined in the articles referred to. Instead, incorrectly defined results fitted their "advice" better.FONTE: http://forum.lowcarb...ad.php?t=423716 Ainda duvida? Postei vários estudos cientificos durante a discussao desse topico, entao vá lendo pagina por pagina que voce encontrará, se nao for o suficiente, convido que voce entre nos logs do BB.com e acompanhe, pois muitos de lá seguem e tem corpos extremamente absurdos...vou dar exemplos: Bob, trabalha no grupo Scivation : http://forum.bodybui...php?t=127002603 Lvisaa: http://forum.bodybui...php?t=138008903 Billy e Erick, competidores BB: http://forum.bodybui...php?t=133734251 Manu: http://forum.bodybui...php?t=135924851Obrigado, agradeco a quem ler tudo issoFONTES:Fonte 1 - Estudos sobre metabolismoFonte 2 - Topico oficial sobre IIFYMFonte 3 - Leangains WebsiteFonte 4 - Body recompositon WebsiteFonte 5 - Alan Aragorn Editado Setembro 15, 2014 às 20:53 por Hipertrofia.org J_Antonaci, Bibiano, thalesgodoy e 58 outros reagiu a isso 61 Link para o comentário Compartilhar em outros sites More sharing options...
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