bassitos

Mais um fato a favor (: Agradeco a todos aquels que estao ajudando aqui tbm, dando mais credibilidade ao tema... Como dito aqui em cima pelo Diego...alimentos processados sao carentes em micronutrientes, nunca disse nada sobre só comer sorvete ou só comer besteiras, porém encaixa-las em seu consumo calorico, para voce manter uma sanidade, conforto e ainda possuir uma otima dieta Se muitos nao sabem como ''comercar'', eu sugiro que comecem fazendo uma regra que muitas pessoas gostam de comecar, para ter controle de quantos alimentos ''sujos'' a pessoa adiciona na dieta. A regra do 80/20 é muito simples, voce consome pelo menos 80% das suas calorias e macronutrientes de comidas ''limpas'' e os 20% de comidas ''sujas'' Eu já nao fico tao precupado com isso, sei que as vezes meu limite passa de 80 e chega a ser um 70/30 ou até mesmo eu faco 90/10.... Essa forma de controle é muito facil para manter uma dieta ótima, sem precisa fazer dia do lixo, onde vc tem 100/0, e nem sabe quantas calorias ingeriu ou etc Abracos (:

O meu com 100g Aveia, 100g Quark, 150g Leite 1.5%, 8g puding mix e 5g café instantaneo da em torno de 600 kcal.... Macros(aproximados): 10g gordura, 76g Carb e 34g Proteinas Com as coisas que eu adiciono, como frutas, passas, sorvete, chocolate....etc vai para umas 800-1000kcal

Antes de comentar, porque nao leram meu post?

Overnight é gold, velho! Colocar sempre 1/1/1-1,5 é a chave do sucesso Lembrando que 1/1/1-1,5 é 1 parte aveia, 1 parte iogurte, algum queijo neutro(nao é salgado nem doce) ou iogurte e 150g isso, GRAMAS de leite Da para brincar com os macros e com os sabores facil facil!

use 1.5-1.6 como fator de atividade para ver como as coisas vao Provavelmente pode ser entre isso... Sim, é a mesma coisa que vc treinar peito inferior e superior....treine Abs tudo em um dia só...aconselho de 2 a 3 vezes por semana

IIFYM nao é uma dieta Nao importa quantas series e quantos movimentos vc faz, o que conta é sua vida tbm fora da academia, conte dias de academia como dias de exercicio E abdomem é um musculo qualquer, se vc treinar todo dia nao vai adiantar nada! Quantos dias por semana voce treina? Como é sua vida fora da academia? Descreve um dia básico seu para poder ajudar

http://translate.google.com.br/translate?sl=en&tl=pt&js=n&prev=_t&hl=de&ie=UTF-8&layout=2&eotf=1&u=http%3A%2F%2Fwww.emma-leigh.com%2Fbasics_dieting_myths.html joguei no tradutor do google....mas se voce puder, leia em ingles

Boas fontes de gordura sao: ovos, castanhas, azeite de oliva, carne vermelha, nozes, amendoas, peixes gordurosos, bacon, queijos.... Sugiro que voce use um desses para criar sua dieta: http://caloriecount.about.com/ http://www.myfitnesspal.com/ http://fatsecret.com/ Se nao quiser, aqui voce encontra dados corretos: http://nutritiondata.self.com

Nao, nao há diferenca quando voce come algum macronutrientes(gordura,carbo ou proteina), o que importa é a nutricao ao final do dia Nao há concetracao ideal para carbos, voce pode comer todos antes de dormir, continuar em deficit calorico que voce nao ganhar gordura...pois voce está gastando mais energia do que consumindo, nao é? logica simples! Sugiro que leia: http://www.hipertrofia.org/forum/topic/50050-iifym-se-encaixa-no-seus-macronutrientes/

Falar comida nao adianta em nada, seu corpo nao ve a diferenca entre uma maca e um pao integral. Ele apenas enxerga o que fi resultante da digestao Só de olhar essa dieta, eu vi que voce nao consome micronutrientes necessarios e utiliza maldodexLIXO apos treino, uma coisa totalmente desnecessaria Sugiro que voce comece a contar calorias e macronutrientes para um melhor aproveitamento Pode comercar lendo aqui http://www.hipertrofia.org/forum/topic/50050-iifym-se-encaixa-no-seus-macronutrientes

Sua dieta é deficiente em gorduras, o que pode gerar problemas hormonais para voce futuramente Há algum motivo por comer de 3 me 3 horas mais ou menos? Para manter seu metabolismo em chamas? Além disso só de ler essa dieta eu passei fome, suas escolhas de alimentos sao muito ruins, e além disso voce gasta muito em suplementos Nao há necessidade de usplementar com BCAA pre e pos se voce possui alimentacao antes e apos...além do mais 2 g de BCAA nao sao nada! voce gasta carboidratos usando maltodextrina pos treino, voce nao possui nenhuma vantagem disso, se voce acha que existe uma tal de janela anabolica, voce esta errado Sugiro que comece lendo: http://www.hipertrofia.org/forum/topic/50050-iifym-se-encaixa-no-seus-macronutrientes/ Abracos!

Se voce nao tem dinheiro para suplementos, apenas coma comida, eles nao sao nada magicos e nao farao a diferenca se voce come suficientemente.... Esse negocio de nao ingerir gordura pos é mentira, o que importa é o que voce comeu no final do dia, nao importa se foi pre, pos, durante ou muito tempo depois Olhando sua dieta eu vejo que é deficiente em micronutrientes, portanto sugiro que voce adicione mais vegetais verdes, saladas, etc.... sugiro tbm que voce leia isso antes de criar uma dieta: http://www.hipertrofia.org/forum/topic/50050-iifym-se-encaixa-no-seus-macronutrientes/

Quem pediu sobre refeed, aqui tem uma artigo muito interessante:http://www.leangains...r-hedonist.html ele engloba refeeds e cheat days, que na verdade um cheat day deveria ser um refeed, que é apenas criar espaco para carboidratos, por isso as gorduras sao muito baixas nesse dia.... sugiro que leiam, vale a pena

Seu corpo nao vai ter nem digerido o almoco ainda.... Nao há necessidade desse pre treino, ao menos que voce queira Composicao corporal nao é afetada por pre ou pos treino, porem pela quantidade de macronutrientes, calorias e micronutrientes atingidas ao final do dia

Se suas contas sobre a maintance estao certas, nao vejo nenhum problema, mas como eu disse, nao é assim tbm, comer qualquer coisa, saiba que micronutrientes sao importantes, por isso procure consumir a maioria de produtos nao processados, ricos em micronutrientes....se voce nao sabe o que sao micronutrientes, sao: vitaminas, minerais, etc... IG varia muito mesmo! Mesmo os testes feitos com pacientes em jejum podem variar com os alimentos consumidos, mesmo vc consumindo um cereal pos treino em jejum, e voce adicionar leite, nao vai ter o mesmo efeito do que so o cereal ou acucar... Nao sei seus status para saber, voce pode tentar um clean bulking ou algo do tipo, ou comer na maintance para saber o que acontece com seu corpo em 2 ate 4 semanas Bcaa nao é totalmente necessario, mas há MUITAS contradicoes, mas é recomendado pelo fundador da dieta...e eu uso sim...19g de Purple Wraath(isso tem aproximadamente 10g de BCAA) de pre treino com 2 caps de cafeína, porque nao consigo tomar café, pois saio da escola direto para a academia Bem vindo ao clube em jejum! jack3d é um perigo, sugiro que nao use mais produtos com 1,3 DMA apos issso por um BOM TEMPO! Mas se vc vai usar, toma o jack 30 mins antes e o bcaa 15 mins antes ou intra treino (:

http://s1111.photobucket.com/albums/h477/bassitos/ album fresquinho com todas comidas desde um bomm tempoo (:

Como foi pedido.... Proteina: +/- 230 (aprox. 3g por Kg.) -> Minimo alcancado...ok! Carboidrato: +/- 380 (aprox. 5g por Kg) Gordura: +/- 100g (aprox. 1,5g por Kg) -> Minimo ultrapassado....ok! Kcal: 3200 (meu TMB é +/- 2800 dia) -> 400kcal de surplus, para ganhos limpos...ok! Voce pode diiminuir gorduras e adicionar carbs se voce desejar, apenas questao de preferencia (: Contanto que voce adquira micronutrientes necessarios, sua dieta esta tudo ok Mas devo complementar com algumas dicas: 1- Voce nao tira vantagem nenhuma comendo 7 refs ao dia...se for sua preferencia pessoa, sem problemas 2- Nao se apegue com tempo de pos liquido, pos solido...nao existe uma janela anabolica de 30 minutos ou algo do tipo, ela dura 24h apos o treino, ou seja, voce treinando em dias seguidos, voce está com a janela sempre aberta (: 3- Acho que voce gasta MUITO em suplemento....nao há necessidade de suplementacao de whey se voce atinge suas necessidades proteicas sem suplemento. Maltodextrina é lixo, assim como dextrose, etc....nao há vantagem alguma e pico de insulina é coisa do passado. Só para seu saber, proteina sozinha ja faz com que a insulina se eleve 4- Nao há necessidade de suplementar com albumina de noite, coma uma refeicao normal, voce nao vai entrar em catabolismo durante a noite 5- Sugiro que voce nao compre mais suplementos e procure investir em alimentacao, a nao ser que voce nao consiga atingir com alimentos, ai sim necessita de suplementos...porém há excessoes como o caso de creatine, mas isso é individual, eu nao vi resultados quando tomei, porem muitos veem, entao seria o unico suplemento ''necessario'' 6- acho que eu ja disse, mas repito denovo, nao ha necessiade de se preucupar com alimentacao de baixo ou alto IG ao menos que voce seja diabetico...o que realmente importa é a nutricao ao final do dia... abracos e boa sorte (:

Eu diminuiria as kcal, tem muita ae, que pode resultar em ganho excessivo de gordura Posso perguntar por que voce faz 9 refeicoes ao dia? Aconselho a voce diminuir as kcal, diminuir proteina e adicionar gordura até 1g/kg.... voce tbm nao come nenhum vegetal verde ou algum tipo de salada, provavelmente sua dieta deve faltar certos micronutrientes Sugiro que voce leia: http://www.hipertrofia.org/forum/topic/50050-iifym-se-encaixa-no-seus-macronutrientes/

HAEUHEUHUAHEUAHE Como o Craw disse, paranoia é a chave para falhar um artigo muito bom sobre isso pode ser lido aqui: http://www.leangains.com/2010/01/marshmallow-test.html

-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.html INTRODUCTION. 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...urated-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...urated-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.html Did 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 HAHAHA

diria de 12 HEUAHUAHEUHAE Sites para voces buscarem receitas criativas e que tem macronutrientes muito bons Sheila's LiveWell 360 Food of April For The Love Of Cookies! Teresa Cutter - The Healthy Chef! Susan Jane Murray - Eating with Intolerences Receitas para pessoas com alergias a alguns ingredientes Pimp My ProteinShake! Diet, Desserts, and Dogs! Muitas receitas variadas Heather Eats Almond Butter Nao só de manteiga de amendoas Kath Eats Real Food YUMMMMMM! Peanut Butter Boy Tudo com manteiga de amendoim! Stuff I make my Husband Algumas interessantes! Pimp My Protein Shake Protein based tastiness - and not just shakes! Couched Add together a unique combination of ingredients with a creative mind and you get awesome ideas for those on restricted diets. Well worth the look! Para quem se interessar por mais pesquisas: Research Database Directory Se voces precisarem de algo, a database deles é imensa, apenas procurar Pubmed Um dos melhores e mais faceis, com estudos sérios, com conclusoes, objetivos, etc HighWire Press BioMed Central Jornais abertos com pesquisas Free Medical Journals Um resumo grátis dos textos Alan Aragon's Research Review Alan, um dos melhores!

100g Frango 200g Molho de tomate 70g Cebola 250g Cogumelo Sal, Pimenta, Curry, Paprika(pimentao) em pó e adocante liquido Esquenta a chapa ou frigideira, adiciona o cogumelo até ele ficar seco, reserva. Frita a cebola, adiciona o frango, depois o cogumelo denovo, coloca o molho vermelho, os temperos e o adocante...espera engrossar que fica pronto..

Churrascaria foi tenso...aqui nao tem isso nao ):

Foi o que eu ja disse, sua dieta é deficiente em gordura e tem excesso de proteina....

Antes de virem xingarem, sem saber como eu comecei, qual é a minha situacao, eu so digo que conhecimento nao tem a ver com corpo, entao eu sugiro que voces comecem a treinar suas mentes antes de criticar Nao aconselho ninguem a seguir, mas um exemplo de deita é leangains.com., sugiro que leiam beem os posts antes de falar algo E também leiam isso: 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. Algo mais detalhado, leiam aqui: 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. Obrigado (: